PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 3860730-4 1985 These data suggest that the phenotypic changes induced by calcitriol in HL-60 cells are consistent with myelomonocytic differentiation in that the resultant cells possess characteristics of both monocytes (morphology, non-specific esterase staining, high levels of AML-2-23 reactivity) and granulocytes (PMN 29 binding, decreased Fc receptors for IgGl, absence of class II HLA antigens). Calcitriol 58-68 RUNX family transcription factor 3 Homo sapiens 265-270 2441245-4 1987 As with the AML-2-23 MoAb, the anti-My23 MoAbs immunoprecipitated a 50,000-55,000 protein from calcitriol treated HL-60 cells. Calcitriol 95-105 RUNX family transcription factor 3 Homo sapiens 12-17 3098477-6 1986 In fact, both the enhancement of Class I and Class II MHC antigen expression and the suppression of AML-2-23 antigen by IFN-gamma were often more profound in the presence of DEX. Dexamethasone 174-177 RUNX family transcription factor 3 Homo sapiens 100-105 3894519-2 1985 Cells of the HL-60 human promyelocytic cell line, when cultured in the presence of 1,25-dihydroxyvitamin D3 (calcitriol), express a surface protein of approximately 50 to 55 kilodaltons (Kd) which was immunoprecipitated with the AML-2-23 MoAb. Calcitriol 83-107 RUNX family transcription factor 3 Homo sapiens 229-234 3894519-3 1985 Furthermore, after 2 days of exposure to calcitriol, HL-60 cells began to release My23 into culture medium, as determined by the ability of culture supernatant from these cells to block the binding of AML-2-23 to myeloid cells. Calcitriol 41-51 RUNX family transcription factor 3 Homo sapiens 201-206 1062226-3 1976 When rubidazone was employed to treat the first attack, complete remission was achieved in : 1) 40 out of 70 patients (57%) with AML; 2) two out of six patients with AML where previous chemotherapy had failed; 3) four out of five patients with ALL; 4) 12 out of 14 patients with acute monoblastic leukemia. zorubicin 5-15 RUNX family transcription factor 3 Homo sapiens 129-135 1062226-4 1976 When used to treat relapse, rubidazone produced complete remission in : 1) 14 out of 31 cases of AML; 2) 18 out of 39 cases of ALL; 3) 2 out of 3 cases of non-Hodgkin lymphoma. zorubicin 28-38 RUNX family transcription factor 3 Homo sapiens 97-103 33444684-3 2021 Here, we show that two seR3s, tandemly-located at 59- and 70-kb upstream of RUNX3 transcription start site, named seR3 -59h and seR3 -70h, are required for RUNX3 expression and cell proliferation in Epstein-Barr virus (EBV)-positive malignant B cells. ser3s 23-28 RUNX family transcription factor 3 Homo sapiens 76-81 33444684-3 2021 Here, we show that two seR3s, tandemly-located at 59- and 70-kb upstream of RUNX3 transcription start site, named seR3 -59h and seR3 -70h, are required for RUNX3 expression and cell proliferation in Epstein-Barr virus (EBV)-positive malignant B cells. ser3s 23-28 RUNX family transcription factor 3 Homo sapiens 156-161 33444684-5 2021 Excision of either or both seR3s by employing CRISPR/Cas9 system resulted in the decrease in RUNX3 expression and the subsequent suppression of cell proliferation and colony forming capability. ser3s 27-32 RUNX family transcription factor 3 Homo sapiens 93-98 33444684-7 2021 These findings suggest that seR3s play a pivotal role in expression and biological function of both RUNX3 and MYC. ser3s 28-33 RUNX family transcription factor 3 Homo sapiens 100-105 33129959-7 2021 Furthermore, miR-20a-5p promoted the development of cervical cancer via targeting RUNX3. mir-20a-5p 13-23 RUNX family transcription factor 3 Homo sapiens 82-87 32460059-3 2020 The results indicated that metformin suppressed the in vitro growth of four leukemia cell lines, OCI/AML2, OCI/AML3, THP-1, and K562, in a dose-dependent manner, which corresponded to the downregulation of the expression and phosphorylation of AXL and inhibition of its downstream targets such as phosphorylation of STAT3. Metformin 27-36 RUNX family transcription factor 3 Homo sapiens 101-105 33440396-3 2021 Although methylated runt-related transcription factor 3 (RUNX3) is a biomarker of pancreatic cancer, its detection by conventional bisulfite-based methylation assays from a small serum sample amount is very difficult. hydrogen sulfite 131-140 RUNX family transcription factor 3 Homo sapiens 20-55 33440396-3 2021 Although methylated runt-related transcription factor 3 (RUNX3) is a biomarker of pancreatic cancer, its detection by conventional bisulfite-based methylation assays from a small serum sample amount is very difficult. hydrogen sulfite 131-140 RUNX family transcription factor 3 Homo sapiens 57-62 32945424-13 2020 In conclusion, miR-130a-3p promoted proliferation, migration and invasion, and inhibited the apoptosis of CC cells via targeting RUNX3, suggesting a novel treatment target for CC. mir-130a-3p 15-26 RUNX family transcription factor 3 Homo sapiens 129-134 32801881-7 2020 Furthermore, treatment with AZA not only promoted the demethylation of RUNX3 but also restored the mRNA and protein expression of RUNX3, and the reactivation of expression of the later exhibited its anti-tumor effects through regulation of the cycle progression in PCa cells. Azathioprine 28-31 RUNX family transcription factor 3 Homo sapiens 71-76 32801881-7 2020 Furthermore, treatment with AZA not only promoted the demethylation of RUNX3 but also restored the mRNA and protein expression of RUNX3, and the reactivation of expression of the later exhibited its anti-tumor effects through regulation of the cycle progression in PCa cells. Azathioprine 28-31 RUNX family transcription factor 3 Homo sapiens 130-135 33482905-0 2021 CAMK2N1/RUNX3 methylation is an independent prognostic biomarker for progression-free and overall survival of platinum-sensitive epithelial ovarian cancer patients. Platinum 110-118 RUNX family transcription factor 3 Homo sapiens 8-13 33482905-3 2021 RESULTS: The marker combination CAMK2N1/RUNX3 exhibited a significant prognostic value for progression-free (PFS) and overall survival (OS) of sporadic platinum-sensitive EOC (n = 188) both in univariate Kaplan-Meier (LogRank p < 0.05) and multivariate Cox regression analysis (p < 0.05; hazard ratio HR = 1.587). Platinum 152-160 RUNX family transcription factor 3 Homo sapiens 40-45 33482905-8 2021 CONCLUSION: The retrospective analysis of 188 sporadic platinum-sensitive EOC proved an independent prognostic value of the methylation marker combination CAMK2N1/RUNX3 for PFS and OS. Platinum 55-63 RUNX family transcription factor 3 Homo sapiens 163-168 33115981-7 2020 In a urethane-induced mouse lung tumor model that recapitulates the features of K-RAS-driven human lung tumors, Runx3 was inactivated in both adenomas (ADs) and ADCs, whereas K-RAS was activated only in ADCs. Urethane 5-13 RUNX family transcription factor 3 Homo sapiens 112-117 32759296-9 2020 A marked enrichment of the transcription factor Runx3 as well as TET2 and TET3 was observed within proximal KIR promoters in CD56bright NK cells cultured with ascorbic acid. Ascorbic Acid 159-172 RUNX family transcription factor 3 Homo sapiens 48-53 32224873-5 2020 Methylated RUNX3 is a well-known biomarker of gastric cancer but it is very difficult to detect with conventional bisulfite-based methylation assays when only a small amount of serum is available. hydrogen sulfite 114-123 RUNX family transcription factor 3 Homo sapiens 11-16 31609478-11 2020 Mechanistically, NO -induced IDO1/Kynurenine/AHR signaling was mediated by RUNX3 transcription factor. Kynurenine 35-45 RUNX family transcription factor 3 Homo sapiens 76-81 31609478-12 2020 Our findings identified a novel NO /RUNX3/Kynurenine metabolic axis, which enhances disease aggressiveness in pancreatic cancer and may have potential translational significance in improving disease outcome. Kynurenine 43-53 RUNX family transcription factor 3 Homo sapiens 37-42 31555951-8 2020 The reactivation of apoptosis-related genes, such as RUNX3, PYCARD, TNF, FAS, and FASLG, was induced by pre-treatment with 5-aza-dC, and the DNA demethylation of promoter CpG islands of RUNX3 and PYCARD was confirmed. decitabine 123-131 RUNX family transcription factor 3 Homo sapiens 53-58 31555951-8 2020 The reactivation of apoptosis-related genes, such as RUNX3, PYCARD, TNF, FAS, and FASLG, was induced by pre-treatment with 5-aza-dC, and the DNA demethylation of promoter CpG islands of RUNX3 and PYCARD was confirmed. decitabine 123-131 RUNX family transcription factor 3 Homo sapiens 186-191 31757777-0 2019 Ethanol promotes alcohol-related colorectal cancer metastasis via the TGF-beta/RUNX3/Snail axis by inducing TGF-beta1 upregulation and RUNX3 cytoplasmic mislocalization. Ethanol 0-7 RUNX family transcription factor 3 Homo sapiens 79-84 31757777-10 2019 INTERPRETATION: Alcohol intake plays a vital role in CRC metastasis via the ethanol-mediated TGF-beta/RUNX3/Snail axis, and PFD might be a novel therapeutic management strategy for CRC. Ethanol 76-83 RUNX family transcription factor 3 Homo sapiens 102-107 31757777-0 2019 Ethanol promotes alcohol-related colorectal cancer metastasis via the TGF-beta/RUNX3/Snail axis by inducing TGF-beta1 upregulation and RUNX3 cytoplasmic mislocalization. Ethanol 0-7 RUNX family transcription factor 3 Homo sapiens 135-140 31757777-0 2019 Ethanol promotes alcohol-related colorectal cancer metastasis via the TGF-beta/RUNX3/Snail axis by inducing TGF-beta1 upregulation and RUNX3 cytoplasmic mislocalization. Alcohols 17-24 RUNX family transcription factor 3 Homo sapiens 79-84 31757777-0 2019 Ethanol promotes alcohol-related colorectal cancer metastasis via the TGF-beta/RUNX3/Snail axis by inducing TGF-beta1 upregulation and RUNX3 cytoplasmic mislocalization. Alcohols 17-24 RUNX family transcription factor 3 Homo sapiens 135-140 31757777-8 2019 Alcohol intake significantly promoted CRC metastasis via the ethanol-mediated TGF-beta/Smad/Snail axis, and ethanol induced the cytoplasmic mislocalization of RUNX3 and further promoted the aggressiveness of CRC by targeting Snail. Ethanol 108-115 RUNX family transcription factor 3 Homo sapiens 159-164 31757777-10 2019 INTERPRETATION: Alcohol intake plays a vital role in CRC metastasis via the ethanol-mediated TGF-beta/RUNX3/Snail axis, and PFD might be a novel therapeutic management strategy for CRC. Alcohols 16-23 RUNX family transcription factor 3 Homo sapiens 102-107 31485638-8 2019 In addition, the results indicated that miR-301a-3p may regulate the Wnt signaling pathway, and rescue experiments indicated that RUNX3 contributed to the effects of miR-301a-3p on cell proliferation and invasion through Wnt signaling. 301a 44-48 RUNX family transcription factor 3 Homo sapiens 130-135 31467531-10 2019 Weighty lower RUNX3 protein level was observed in GMB specimens compared to grade II-III astrocytomas. N-(gamma-maleimidobutyryloxy)succinimide 50-53 RUNX family transcription factor 3 Homo sapiens 14-19 30982493-5 2019 miR-148-3p mimics effectively suppressed the expression of DNMT1 and methylation of RUNX3 promoter, finally upregulating RUNX3 expression. mir-148-3p 0-10 RUNX family transcription factor 3 Homo sapiens 84-89 30982493-5 2019 miR-148-3p mimics effectively suppressed the expression of DNMT1 and methylation of RUNX3 promoter, finally upregulating RUNX3 expression. mir-148-3p 0-10 RUNX family transcription factor 3 Homo sapiens 121-126 30982493-8 2019 In conclusion, miR-148-3p directly repressed the expression of DNMT1 and inhibited proliferation, migration, and invasion by regulating DNMT1-RUNX3 axis and the epithelial-mesenchymal transition in GBM. mir-148-3p 15-25 RUNX family transcription factor 3 Homo sapiens 142-147 30650190-0 2019 Genetic variants in RUNX3, AMD1 and MSRA in the methionine metabolic pathway and survival in nonsmall cell lung cancer patients. Methionine 48-58 RUNX family transcription factor 3 Homo sapiens 20-25 30593754-8 2018 Both polymorphisms influenced the methylation status, carriers of OGG1 326Ser/Cys or Ser/Cys+Cys/Cys genotypes demonstrating increased frequency of methylated RUNX3 and ISL1 genes whereas the similar effect of XRCC1 polymorphism concerning methylation of p16 and TIMP3 genes. 326ser 71-77 RUNX family transcription factor 3 Homo sapiens 159-164 30760870-5 2019 Interaction with RUNX1 and RUNX3 inhibits CRBN-dependent binding, ubiquitylation, and degradation of IKZF1 and IKZF3 upon lenalidomide treatment. Lenalidomide 122-134 RUNX family transcription factor 3 Homo sapiens 27-32 30692634-5 2019 Overexpression of RUNX3 increased DR5 expression via induction of the reactive oxygen species (ROS)-endoplasmic reticulum (ER) stress-effector CHOP. Reactive Oxygen Species 70-93 RUNX family transcription factor 3 Homo sapiens 18-23 30692634-5 2019 Overexpression of RUNX3 increased DR5 expression via induction of the reactive oxygen species (ROS)-endoplasmic reticulum (ER) stress-effector CHOP. Reactive Oxygen Species 95-98 RUNX family transcription factor 3 Homo sapiens 18-23 30692634-7 2019 Interestingly, RUNX3 induced reactive oxygen species production by inhibiting SOD3 transcription via binding to the Superoxide dismutase 3 (SOD3) promoter. Reactive Oxygen Species 29-52 RUNX family transcription factor 3 Homo sapiens 15-20 30858545-7 2019 Mechanistically, miR-339-5p enhances radiosensitivity by targeting Cdc25A, and is transcriptionally regulated by Runx3. mir-339-5p 17-27 RUNX family transcription factor 3 Homo sapiens 113-118 30858545-8 2019 Correlations were observed between miR-339-5p levels and Cdc25A/Runx3 levels in tissue samples. mir-339-5p 35-45 RUNX family transcription factor 3 Homo sapiens 64-69 30593754-8 2018 Both polymorphisms influenced the methylation status, carriers of OGG1 326Ser/Cys or Ser/Cys+Cys/Cys genotypes demonstrating increased frequency of methylated RUNX3 and ISL1 genes whereas the similar effect of XRCC1 polymorphism concerning methylation of p16 and TIMP3 genes. Cysteine 89-92 RUNX family transcription factor 3 Homo sapiens 159-164 30593754-8 2018 Both polymorphisms influenced the methylation status, carriers of OGG1 326Ser/Cys or Ser/Cys+Cys/Cys genotypes demonstrating increased frequency of methylated RUNX3 and ISL1 genes whereas the similar effect of XRCC1 polymorphism concerning methylation of p16 and TIMP3 genes. Cysteine 78-81 RUNX family transcription factor 3 Homo sapiens 159-164 30593754-8 2018 Both polymorphisms influenced the methylation status, carriers of OGG1 326Ser/Cys or Ser/Cys+Cys/Cys genotypes demonstrating increased frequency of methylated RUNX3 and ISL1 genes whereas the similar effect of XRCC1 polymorphism concerning methylation of p16 and TIMP3 genes. Serine 74-77 RUNX family transcription factor 3 Homo sapiens 159-164 30593754-8 2018 Both polymorphisms influenced the methylation status, carriers of OGG1 326Ser/Cys or Ser/Cys+Cys/Cys genotypes demonstrating increased frequency of methylated RUNX3 and ISL1 genes whereas the similar effect of XRCC1 polymorphism concerning methylation of p16 and TIMP3 genes. Cysteine 89-92 RUNX family transcription factor 3 Homo sapiens 159-164 30593754-8 2018 Both polymorphisms influenced the methylation status, carriers of OGG1 326Ser/Cys or Ser/Cys+Cys/Cys genotypes demonstrating increased frequency of methylated RUNX3 and ISL1 genes whereas the similar effect of XRCC1 polymorphism concerning methylation of p16 and TIMP3 genes. Cysteine 89-92 RUNX family transcription factor 3 Homo sapiens 159-164 30258965-11 2018 Moreover, the signal axis of Rarb/Runx3/Col6a1 is pharmaceutically accessible to a widely used antidiabetic substance, metformin, and Rar modulator. Metformin 119-128 RUNX family transcription factor 3 Homo sapiens 34-39 30178853-12 2018 Overexpression of Runx3 reversed the miR-19b knockdown-induced Caco2 cell viability inhibition, apoptosis enhancement, inflammatory factors expressions and NF-kappaB and PI3K/AKT signaling pathways activation. caco2 63-68 RUNX family transcription factor 3 Homo sapiens 18-23 30178853-13 2018 CONCLUSIONS: Our study demonstrated that miR-19b alleviated LPS-induced Caco2 cell inflammatory injury via up-regulation of Runx3 and deactivation of NF-kappaB and PI3K/AKT signaling pathways. caco2 72-77 RUNX family transcription factor 3 Homo sapiens 124-129 29983874-4 2018 Methods: The sensitivity to sorafenib-induced cell death (MTT test and anexin V/7-AAD method) was evaluated in five different cell lines: MOLM-13, OCI-AML2, HL-60, HEL and K-562. Sorafenib 28-37 RUNX family transcription factor 3 Homo sapiens 151-155 29983874-7 2018 Results: The cytostatic response to sorafenib was: MOLM-13>>OCI-AML2>HL-60>HEL K-562. Sorafenib 36-45 RUNX family transcription factor 3 Homo sapiens 70-74 29983874-11 2018 The expression of the organic cation transporter 1 (OCT1), involved in sorafenib uptake, was MOLM-13>OCI-AML2 HL-60 and non detectable in HEL and K-562. Sorafenib 71-80 RUNX family transcription factor 3 Homo sapiens 108-112 29693143-6 2018 The demethylating agent 5-aza-2"-deoxycytidine (ADC) was used to reverse the methylation of the RUNX3 promoter. Decitabine 24-46 RUNX family transcription factor 3 Homo sapiens 96-101 29693143-6 2018 The demethylating agent 5-aza-2"-deoxycytidine (ADC) was used to reverse the methylation of the RUNX3 promoter. adc 48-51 RUNX family transcription factor 3 Homo sapiens 96-101 29342962-8 2018 RUNX3 exhibited dualistic functions related to cisplatin sensitivity and migration capacity, depending on the respective transcript variant (TV). Cisplatin 47-56 RUNX family transcription factor 3 Homo sapiens 0-5 29499952-12 2018 In conclusion, downregulating PIWIL1 and piR-DQ593109 increased BTB permeability through the MEG3/miR-330-5p/RUNX3 axis. btb 64-67 RUNX family transcription factor 3 Homo sapiens 109-114 29342962-9 2018 A2780 cells expressing RUNX3 TV2-the promoter of which harbors a CpG (5"-C-phosphate-G-3") island and is potentially inactivated by hypermethylation-exhibited increased cisplatin sensitivity and reduced migration properties. Cisplatin 169-178 RUNX family transcription factor 3 Homo sapiens 23-28 28699703-0 2017 A positive feedback loop promotes HIF-1alpha stability through miR-210-mediated suppression of RUNX3 in paraquat-induced EMT. Paraquat 104-112 RUNX family transcription factor 3 Homo sapiens 95-100 28699703-8 2017 Runt-related transcription factor-3 (RUNX3), a direct target of miR-210, was inhibited by miR-210 in response to PQ poisoning. Paraquat 113-115 RUNX family transcription factor 3 Homo sapiens 0-35 28699703-8 2017 Runt-related transcription factor-3 (RUNX3), a direct target of miR-210, was inhibited by miR-210 in response to PQ poisoning. Paraquat 113-115 RUNX family transcription factor 3 Homo sapiens 37-42 28699703-14 2017 The mechanism may function through miR-210-mediated repression of RUNX3, which further decreases the hydroxylation activity of PHD2, enhances the stability of HIF-1alpha, and promotes PQ-induced EMT, aggravating the progression of pulmonary fibrosis. Paraquat 184-186 RUNX family transcription factor 3 Homo sapiens 66-71 29340016-6 2017 Down-regulation of miR-19 dramatically inhibited proliferation, invasion and induced the cell cycle G1 arrest and apoptosis, at least partly via the up-regulation of RUNX3. mir-19 19-25 RUNX family transcription factor 3 Homo sapiens 166-171 28958164-2 2017 Here, we report that doxorubicin encapsulated in lipoic acid-crosslinked hyaluronic acid nanoparticles (LACHA-DOX) mediate highly efficacious and targeted inhibition of human hematological cancers including LP-1 human multiple myeloma (MM) and AML-2 human acute myeloid leukemia xenografted in nude mice. Doxorubicin 21-32 RUNX family transcription factor 3 Homo sapiens 244-249 29340016-0 2017 MiR-19 regulates the proliferation and invasion of glioma by RUNX3 via beta-catenin/Tcf-4 signaling. mir-19 0-6 RUNX family transcription factor 3 Homo sapiens 61-66 28958164-2 2017 Here, we report that doxorubicin encapsulated in lipoic acid-crosslinked hyaluronic acid nanoparticles (LACHA-DOX) mediate highly efficacious and targeted inhibition of human hematological cancers including LP-1 human multiple myeloma (MM) and AML-2 human acute myeloid leukemia xenografted in nude mice. Thioctic Acid 49-60 RUNX family transcription factor 3 Homo sapiens 244-249 28958164-2 2017 Here, we report that doxorubicin encapsulated in lipoic acid-crosslinked hyaluronic acid nanoparticles (LACHA-DOX) mediate highly efficacious and targeted inhibition of human hematological cancers including LP-1 human multiple myeloma (MM) and AML-2 human acute myeloid leukemia xenografted in nude mice. Hyaluronic Acid 73-88 RUNX family transcription factor 3 Homo sapiens 244-249 28958164-2 2017 Here, we report that doxorubicin encapsulated in lipoic acid-crosslinked hyaluronic acid nanoparticles (LACHA-DOX) mediate highly efficacious and targeted inhibition of human hematological cancers including LP-1 human multiple myeloma (MM) and AML-2 human acute myeloid leukemia xenografted in nude mice. lacha-dox 104-113 RUNX family transcription factor 3 Homo sapiens 244-249 28958164-6 2017 MTT and flow cytometry assays showed that LACHA-DOX possessed a high targetability and antitumor activity toward CD44 receptor overexpressing LP-1 human MM cells and AML-2 human acute myeloid leukemia cells. lacha-dox 42-51 RUNX family transcription factor 3 Homo sapiens 166-171 27766776-0 2016 RUNX3 reverses cisplatin resistance in esophageal squamous cell carcinoma via suppression of the protein kinase B pathway. Cisplatin 15-24 RUNX family transcription factor 3 Homo sapiens 0-5 28542846-3 2017 CIMP status was determined by analyzing the 5-markers CAGNA1G, IGF2, NEUROG1, RUNX3 and SOCS1 by quantitative methylation specific PCR (qMSP). Cyclic IMP 0-4 RUNX family transcription factor 3 Homo sapiens 78-83 27990641-4 2017 The cytoplasmic localization of RUNX3 was associated with oxidative stress-induced RUNX3 phosphorylation at tyrosine residues via SRC activation. Tyrosine 108-116 RUNX family transcription factor 3 Homo sapiens 32-37 27990641-4 2017 The cytoplasmic localization of RUNX3 was associated with oxidative stress-induced RUNX3 phosphorylation at tyrosine residues via SRC activation. Tyrosine 108-116 RUNX family transcription factor 3 Homo sapiens 83-88 28458013-13 2017 Taken together, these observations suggest that aberrant methylation of RUNX3 and LINE-1 might be involved in AFB1-induced carcinogenesis. Aflatoxin B1 110-114 RUNX family transcription factor 3 Homo sapiens 72-77 28498402-8 2017 RUNX3 expression was reduced in si-RUNX3 and si-RUNX3+DAPT group but the expression levels of Notch signaling related genes were markedly increased in si-RUNX3 group or decreased in DAPT and si-NC+DAPT group, as compared with those in the control group (all P<0.05). dapt 54-58 RUNX family transcription factor 3 Homo sapiens 0-5 27430892-4 2017 The promoter regions of p73 and RUNX3 were demethylated, and their expression was up-regulated by decitabine. Decitabine 98-108 RUNX family transcription factor 3 Homo sapiens 32-37 27646854-9 2016 A pronounced demethylating effect of guadecitabine was obtained also in the promoters of a subset of tumor suppressors genes (CDKN2A, DLEC1, and RUNX3) in HepG2 and Huh-7 HCC cells. guadecitabine 37-50 RUNX family transcription factor 3 Homo sapiens 145-150 28458013-0 2017 Aberrant methylation of RUNX3 is present in Aflatoxin B1-induced transformation of the L02R cell line. Aflatoxin B1 44-56 RUNX family transcription factor 3 Homo sapiens 24-29 28458013-8 2017 The methylated CpG sites of RUNX3 genes were verified using bisulfite sequencing PCR (BSP) assay. hydrogen sulfite 60-69 RUNX family transcription factor 3 Homo sapiens 28-33 28458013-10 2017 In vitro study showed that methylation of RUNX3 tended to abate in L02R cells treated with AFB1 for a short-term period of time. Aflatoxin B1 91-95 RUNX family transcription factor 3 Homo sapiens 42-47 28129457-9 2017 Oxidative MS-PCR analysis detected 5-mC in the PRDM2, RUNX3, and TP73 genes in 10/22 (45%), 15/21 (71%), and 16/26 (62%) samples with methylation detected by MS-PCR, respectively. 5-mc 35-39 RUNX family transcription factor 3 Homo sapiens 54-59 28184917-0 2017 [Corrigendum] Loss of Runt-related transcription factor 3 induces resistance to 5-fluorouracil and cisplatin in hepatocellular carcinoma. Fluorouracil 80-94 RUNX family transcription factor 3 Homo sapiens 22-57 28184917-0 2017 [Corrigendum] Loss of Runt-related transcription factor 3 induces resistance to 5-fluorouracil and cisplatin in hepatocellular carcinoma. Cisplatin 99-108 RUNX family transcription factor 3 Homo sapiens 22-57 28184917-6 2017 Therefore, the subsection entitled "Ectopic RUNX3 protein expression suppresses cell growth..." should have been entitled "Ectopic RUNX3 protein expression increases 5-FU and CDDP sensitivity", and the text herein should have read as follows: We analyzed the effects of RUNX3 on chemosensitivity in the RUNX3- or CAT (mock)-transfected Hep3B and Huh7 cells. Cisplatin 175-179 RUNX family transcription factor 3 Homo sapiens 44-49 28184917-6 2017 Therefore, the subsection entitled "Ectopic RUNX3 protein expression suppresses cell growth..." should have been entitled "Ectopic RUNX3 protein expression increases 5-FU and CDDP sensitivity", and the text herein should have read as follows: We analyzed the effects of RUNX3 on chemosensitivity in the RUNX3- or CAT (mock)-transfected Hep3B and Huh7 cells. Cisplatin 175-179 RUNX family transcription factor 3 Homo sapiens 131-136 28184917-6 2017 Therefore, the subsection entitled "Ectopic RUNX3 protein expression suppresses cell growth..." should have been entitled "Ectopic RUNX3 protein expression increases 5-FU and CDDP sensitivity", and the text herein should have read as follows: We analyzed the effects of RUNX3 on chemosensitivity in the RUNX3- or CAT (mock)-transfected Hep3B and Huh7 cells. Cisplatin 175-179 RUNX family transcription factor 3 Homo sapiens 131-136 28184917-6 2017 Therefore, the subsection entitled "Ectopic RUNX3 protein expression suppresses cell growth..." should have been entitled "Ectopic RUNX3 protein expression increases 5-FU and CDDP sensitivity", and the text herein should have read as follows: We analyzed the effects of RUNX3 on chemosensitivity in the RUNX3- or CAT (mock)-transfected Hep3B and Huh7 cells. Cisplatin 175-179 RUNX family transcription factor 3 Homo sapiens 131-136 28184917-7 2017 RUNX3 expression enhanced 5-FU sensitivity in both cell lines; the cell viability with 5-FU (100 nM) decreased from 66.3+-4.6 to 34.3+-5.0%, and from 71.0+-4.7% to 27.0+-5.5% in the Hep3B and Huh7 cells, respectively (Fig. Fluorouracil 26-30 RUNX family transcription factor 3 Homo sapiens 0-5 28184917-7 2017 RUNX3 expression enhanced 5-FU sensitivity in both cell lines; the cell viability with 5-FU (100 nM) decreased from 66.3+-4.6 to 34.3+-5.0%, and from 71.0+-4.7% to 27.0+-5.5% in the Hep3B and Huh7 cells, respectively (Fig. Fluorouracil 87-91 RUNX family transcription factor 3 Homo sapiens 0-5 28184917-9 2017 RUNX3 expression also enhanced CDDP sensitivity in both cell lines; the cell viability with CDDP (100 nM) decreased from 58.7+-2.6% to 25.7+-4.9%, and from 67.7+-4.1% to 25.7+-7.5% in the Hep3B and Huh7 cells, respectively (Fig. Cisplatin 31-35 RUNX family transcription factor 3 Homo sapiens 0-5 28184917-9 2017 RUNX3 expression also enhanced CDDP sensitivity in both cell lines; the cell viability with CDDP (100 nM) decreased from 58.7+-2.6% to 25.7+-4.9%, and from 67.7+-4.1% to 25.7+-7.5% in the Hep3B and Huh7 cells, respectively (Fig. Cisplatin 92-96 RUNX family transcription factor 3 Homo sapiens 0-5 28011426-0 2017 Improving potency and metabolic stability by introducing an alkenyl linker to pyridine-based histone deacetylase inhibitors for orally available RUNX3 modulators. pyridine 78-86 RUNX family transcription factor 3 Homo sapiens 145-150 28011426-2 2017 Histone deacetylases (HDACs) can deacetylate the lysine residues of RUNX3, followed by degradation via a ubiquitin-mediated pathway. Lysine 49-55 RUNX family transcription factor 3 Homo sapiens 68-73 27793801-6 2016 Interestingly, Runx3 can be synergistically induced by IFNgamma with a synthetic analog of viral dsRNA polyinosinic-polycytidylic acid [poly(I:C)] or tumor necrosis factor-alpha (TNFalpha) through both JAK-STAT1 and NF-kappaB pathways. Poly I-C 103-134 RUNX family transcription factor 3 Homo sapiens 15-20 27498627-0 2016 RUNX3 plays an important role in As2O3-induced apoptosis and allows cells to overcome MSC-mediated drug resistance. Arsenic Trioxide 33-38 RUNX family transcription factor 3 Homo sapiens 0-5 27498627-3 2016 In our study, runt-related transcription factor 3 (RUNX3) was identified as a novel target gene affected by As2O3 and involved in mesenchymal stem cell (MSC)-mediated protection of leukemia cells from As2O3-induced apoptosis. Arsenic Trioxide 108-113 RUNX family transcription factor 3 Homo sapiens 14-49 27498627-3 2016 In our study, runt-related transcription factor 3 (RUNX3) was identified as a novel target gene affected by As2O3 and involved in mesenchymal stem cell (MSC)-mediated protection of leukemia cells from As2O3-induced apoptosis. Arsenic Trioxide 108-113 RUNX family transcription factor 3 Homo sapiens 51-56 27498627-3 2016 In our study, runt-related transcription factor 3 (RUNX3) was identified as a novel target gene affected by As2O3 and involved in mesenchymal stem cell (MSC)-mediated protection of leukemia cells from As2O3-induced apoptosis. Arsenic Trioxide 201-206 RUNX family transcription factor 3 Homo sapiens 14-49 27498627-3 2016 In our study, runt-related transcription factor 3 (RUNX3) was identified as a novel target gene affected by As2O3 and involved in mesenchymal stem cell (MSC)-mediated protection of leukemia cells from As2O3-induced apoptosis. Arsenic Trioxide 201-206 RUNX family transcription factor 3 Homo sapiens 51-56 27498627-4 2016 We observed induction of RUNX3 expression and the translocation of RUNX3 into the nucleus after As2O3 treatment in leukemia cells. Arsenic Trioxide 96-101 RUNX family transcription factor 3 Homo sapiens 67-72 27498627-5 2016 In K562 chronic myeloid leukemia cells, downregulation of endogenous RUNX3 compromised As2O3-induced growth inhibition, cell cycle arrest, and apoptosis. Arsenic Trioxide 87-92 RUNX family transcription factor 3 Homo sapiens 69-74 27498627-6 2016 In the presence of MSC, As2O3-induced expression of RUNX3 was reduced significantly and this reduction was modulated by CXCL12/CXCR4 signaling. Arsenic Trioxide 24-29 RUNX family transcription factor 3 Homo sapiens 52-57 27498627-7 2016 Furthermore, overexpression of RUNX3 restored, at least in part, the sensitivity of leukemic cells to As2O3. Arsenic Trioxide 102-107 RUNX family transcription factor 3 Homo sapiens 31-36 27498627-8 2016 We conclude that RUNX3 plays an important role in As2O3-induced cellular responses and allows cells to overcome MSC-mediated drug resistance. Arsenic Trioxide 50-55 RUNX family transcription factor 3 Homo sapiens 17-22 27766776-3 2016 In this study, the role of RUNX3 in the formation of cisplatin resistance in ESCC was examined. Cisplatin 53-62 RUNX family transcription factor 3 Homo sapiens 27-32 27766776-6 2016 RESULTS: A higher expression of RUNX3 in ESCC patients correlated with a more sensitive response to cisplatin-based chemotherapy. Cisplatin 100-109 RUNX family transcription factor 3 Homo sapiens 32-37 27766776-8 2016 A lower RUNX3 expression in cisplatin-resistant ESCC cell lines, Eca109 and TE-1, was observed compared with parental cell lines. Cisplatin 28-37 RUNX family transcription factor 3 Homo sapiens 8-13 27766776-9 2016 Heterologous RUNX3 expression significantly suppressed cisplatin resistance in Eca109 and TE-1, both in vitro and vivo. Cisplatin 55-64 RUNX family transcription factor 3 Homo sapiens 13-18 27766776-10 2016 Meanwhile, heterologous RUNX3 expression could inhibit growth and induce apoptosis in cisplatin resistant Eca109 and TE-1 cell lines in vitro. Cisplatin 86-95 RUNX family transcription factor 3 Homo sapiens 24-29 27766776-13 2016 CONCLUSION: Our results confirmed that a loss of RUNX3 in ESCC may contribute to cisplatin-resistance. Cisplatin 81-90 RUNX family transcription factor 3 Homo sapiens 49-54 27766776-14 2016 RUNX3 could reverse cisplatin resistance via suppression of the Akt pathway in ESCC patients. Cisplatin 20-29 RUNX family transcription factor 3 Homo sapiens 0-5 26756918-7 2016 Of these smoking-related CpGs, methylation levels at 80 CpGs showed significant correlations with the expression of corresponding genes (including RUNX3, IL6R, PTAFR, ANKRD11, CEP135 and CDH23), and methylation at 15 CpGs was significantly associated with urinary 2-hydroxynaphthalene, the most representative internal monohydroxy-PAH biomarker for smoking. 2-naphthol 264-284 RUNX family transcription factor 3 Homo sapiens 147-152 26756918-7 2016 Of these smoking-related CpGs, methylation levels at 80 CpGs showed significant correlations with the expression of corresponding genes (including RUNX3, IL6R, PTAFR, ANKRD11, CEP135 and CDH23), and methylation at 15 CpGs was significantly associated with urinary 2-hydroxynaphthalene, the most representative internal monohydroxy-PAH biomarker for smoking. monohydroxy-pah 319-334 RUNX family transcription factor 3 Homo sapiens 147-152 27135485-6 2016 Bisulfite-treated DNA was used for methylation testing of RUNX3, COX2, and MINT1. hydrogen sulfite 0-9 RUNX family transcription factor 3 Homo sapiens 58-63 26853927-3 2016 Reduced methylation and increased expression of RUNX3 genes in vitro was observed and decreased cell migration was further confirmed following 5-azacytidine treatment. Azacitidine 143-156 RUNX family transcription factor 3 Homo sapiens 48-53 27217562-4 2016 We show that the phosphorylation of threonine 173 (T173) residue within the Runt domain of RUNX3 disrupts RUNX DNA binding activity during mitotic entry to facilitate the recruitment of RUNX proteins to mitotic structures. Threonine 36-45 RUNX family transcription factor 3 Homo sapiens 91-96 26702772-5 2016 CIMP status was determined using the DNA methylation status of CACNA1G, IGF2, NEUROG1, RUNX3, and SOCS1. Cyclic IMP 0-4 RUNX family transcription factor 3 Homo sapiens 87-92 26985715-0 2016 Loss of Runt-related transcription factor 3 induces resistance to 5-fluorouracil and cisplatin in hepatocellular carcinoma. Fluorouracil 66-80 RUNX family transcription factor 3 Homo sapiens 8-43 26985715-0 2016 Loss of Runt-related transcription factor 3 induces resistance to 5-fluorouracil and cisplatin in hepatocellular carcinoma. Cisplatin 85-94 RUNX family transcription factor 3 Homo sapiens 8-43 26985715-6 2016 MTT assays were used to determine the effects of RUNX3 expression on 5-fluorouracil (5-FU) and cisplatin (CDDP) sensitivity. Fluorouracil 69-83 RUNX family transcription factor 3 Homo sapiens 49-54 26985715-6 2016 MTT assays were used to determine the effects of RUNX3 expression on 5-fluorouracil (5-FU) and cisplatin (CDDP) sensitivity. Fluorouracil 85-89 RUNX family transcription factor 3 Homo sapiens 49-54 26985715-6 2016 MTT assays were used to determine the effects of RUNX3 expression on 5-fluorouracil (5-FU) and cisplatin (CDDP) sensitivity. Cisplatin 95-104 RUNX family transcription factor 3 Homo sapiens 49-54 26985715-10 2016 Importantly, loss of RUNX3 expression contributed to 5-FU and CDDP resistance by inducing MRP expression. Fluorouracil 53-57 RUNX family transcription factor 3 Homo sapiens 21-26 26985715-10 2016 Importantly, loss of RUNX3 expression contributed to 5-FU and CDDP resistance by inducing MRP expression. Cisplatin 62-66 RUNX family transcription factor 3 Homo sapiens 21-26 26392314-8 2015 In LO2 - RUNX3 (low), the rate of cell proliferation and the level of cisplatin resistance were the same as in the LO2 -core. Cisplatin 70-79 RUNX family transcription factor 3 Homo sapiens 9-14 26475207-0 2015 FLT3-ITD drives Ara-C resistance in leukemic cells via the induction of RUNX3. Cytarabine 16-21 RUNX family transcription factor 3 Homo sapiens 72-77 26475207-5 2015 The knockdown of the RUNX3 expression in the K562/FLT3-ITD cells increased the sensitivity to Ara-C, and the exogenous expression of RUNX3 per se resulted in the enhancement of Ara-C resistance in the K562 cells. Cytarabine 94-99 RUNX family transcription factor 3 Homo sapiens 21-26 26475207-5 2015 The knockdown of the RUNX3 expression in the K562/FLT3-ITD cells increased the sensitivity to Ara-C, and the exogenous expression of RUNX3 per se resulted in the enhancement of Ara-C resistance in the K562 cells. Cytarabine 177-182 RUNX family transcription factor 3 Homo sapiens 21-26 26475207-5 2015 The knockdown of the RUNX3 expression in the K562/FLT3-ITD cells increased the sensitivity to Ara-C, and the exogenous expression of RUNX3 per se resulted in the enhancement of Ara-C resistance in the K562 cells. Cytarabine 177-182 RUNX family transcription factor 3 Homo sapiens 133-138 26475207-7 2015 Collectively, these findings demonstrate that RUNX3 is a prerequisite for Ara-C resistance via FLT3-ITD signaling. Cytarabine 74-79 RUNX family transcription factor 3 Homo sapiens 46-51 26484416-6 2015 Treatment of OCI-AML2 cells with 10-50 microM 2-C-methyladenosine (2-CM), a chain terminator of mitochondrial transcription, reduced mitochondrial gene expression and oxidative phosphorylation, and increased cell death in a concentration-dependent manner. 2'-C-methyladenosine 46-65 RUNX family transcription factor 3 Homo sapiens 17-21 26367000-8 2015 Gene expression modeling of 6 month biopsies across 7/11 genes (CD6, INPP5D, ISG20, NKG7, PSMB9, RUNX3, and TAP1) significantly (p = 0.037) predicted the development of pIFTA at 24 months. pifta 169-174 RUNX family transcription factor 3 Homo sapiens 97-102 25948105-0 2015 Baicalein increases the expression and reciprocal interplay of RUNX3 and FOXO3a through crosstalk of AMPKalpha and MEK/ERK1/2 signaling pathways in human non-small cell lung cancer cells. baicalein 0-9 RUNX family transcription factor 3 Homo sapiens 63-68 26353591-4 2015 We here introduce a strategy, combination of selective oxidation and bisulfite pyrosequencing (BS-Pyroseq), for quantification of both 5mC and 5hmC at CpG sites within the promoters of CDH1, DAPK, RARbeta and RUNX3 genes in a panel of cell lines and clinical samples. bs-pyroseq 95-105 RUNX family transcription factor 3 Homo sapiens 209-214 25088199-1 2015 Runt domain transcription factor 3 (RUNX3) is widely regarded as a tumour-suppressor gene inactivated by DNA hypermethylation of its canonical CpG (cytidine-phosphate-guanidine) island (CGI) promoter in gastric cancer (GC). Cytosine Nucleotides 148-166 RUNX family transcription factor 3 Homo sapiens 36-41 25088199-1 2015 Runt domain transcription factor 3 (RUNX3) is widely regarded as a tumour-suppressor gene inactivated by DNA hypermethylation of its canonical CpG (cytidine-phosphate-guanidine) island (CGI) promoter in gastric cancer (GC). Guanidine 167-176 RUNX family transcription factor 3 Homo sapiens 36-41 26186909-0 2015 RUNX3 contributes to carboplatin resistance in epithelial ovarian cancer cells. Carboplatin 21-32 RUNX family transcription factor 3 Homo sapiens 0-5 26186909-3 2015 Here, we investigated the role of RUNX3 in carboplatin resistance in EOC cells. Carboplatin 43-54 RUNX family transcription factor 3 Homo sapiens 34-39 26186909-4 2015 METHODS: Expression of RUNX3 was determined in human EOC cell line A2780s (cisplatin-sensitive) and A2780cp (cisplatin-resistant), human ovarian surface epithelium (OSE) and primary EOC cells. Cisplatin 75-84 RUNX family transcription factor 3 Homo sapiens 23-28 26186909-4 2015 METHODS: Expression of RUNX3 was determined in human EOC cell line A2780s (cisplatin-sensitive) and A2780cp (cisplatin-resistant), human ovarian surface epithelium (OSE) and primary EOC cells. Cisplatin 109-118 RUNX family transcription factor 3 Homo sapiens 23-28 26186909-5 2015 The effects of RUNX3 expression on sensitivity to carboplatin were determined in A2780s and A2780cp cells using neutral red uptake and clonogenic assays. Carboplatin 50-61 RUNX family transcription factor 3 Homo sapiens 15-20 26186909-9 2015 Overexpression of RUNX3 rendered A2780s cells more resistant to carboplatin, whereas inhibition of RUNX3 increased sensitivity to carboplatin in A2780cp cells. Carboplatin 64-75 RUNX family transcription factor 3 Homo sapiens 18-23 26186909-9 2015 Overexpression of RUNX3 rendered A2780s cells more resistant to carboplatin, whereas inhibition of RUNX3 increased sensitivity to carboplatin in A2780cp cells. Carboplatin 130-141 RUNX family transcription factor 3 Homo sapiens 99-104 26186909-10 2015 Inhibition of RUNX3 potentiated carboplatin-induced apoptosis in A2780cp cells as demonstrated by more pronounced PARP cleavage. Carboplatin 32-43 RUNX family transcription factor 3 Homo sapiens 14-19 26186909-12 2015 Overexpression of RUNX3 increased cIAP2 expression in A2780s cells, whereas inhibition of RUNX3 decreased cIAP2 expression and potentiated carboplatin-induced decrease of cIAP2 in A2780cp cells. Carboplatin 139-150 RUNX family transcription factor 3 Homo sapiens 90-95 26186909-13 2015 CONCLUSIONS: RUNX3 contributes to carboplatin resistance in EOC cells and may hold promise as a therapeutic target to treat EOC and/or a biomarker to predict chemoresistance. Carboplatin 34-45 RUNX family transcription factor 3 Homo sapiens 13-18 26045321-4 2015 The current research was designed to delineate the mechanism of miR-138 in regulating psoriasis via targeting RUNX3. mir-138 64-71 RUNX family transcription factor 3 Homo sapiens 110-115 26045321-6 2015 Moreover, the luciferase report confirmed the targeting reaction between miR-138 and RUNX3. mir-138 73-80 RUNX family transcription factor 3 Homo sapiens 85-90 26045321-7 2015 After transfection with the miR-138 inhibitor into CD4(+) T cells from healthy controls, we found that the inhibition of miR-138 increases RUNX3 expression and increased the ratio of Th1/Th2. mir-138 28-35 RUNX family transcription factor 3 Homo sapiens 139-144 26045321-7 2015 After transfection with the miR-138 inhibitor into CD4(+) T cells from healthy controls, we found that the inhibition of miR-138 increases RUNX3 expression and increased the ratio of Th1/Th2. mir-138 121-128 RUNX family transcription factor 3 Homo sapiens 139-144 26045321-9 2015 The results showed that the overexpression of miR-138 inhibits RUNX3 expression and decreased the ratio of Th1/Th2 in CD4(+) T cells. mir-138 46-53 RUNX family transcription factor 3 Homo sapiens 63-68 26045321-10 2015 Taken together, our study suggests that increased miR-138 regulates the balance of Th1/Th2 through inhibiting RUNX3 expression in psoriasis, providing a potential therapeutic target for psoriasis. mir-138 50-57 RUNX family transcription factor 3 Homo sapiens 110-115 25948105-10 2015 Baicalein induced RUNX3 and FOXO3a protein expression, and increased phosphorylation of AMPKalpha and ERK1/2. baicalein 0-9 RUNX family transcription factor 3 Homo sapiens 18-23 25948105-11 2015 Moreover, the inhibitors of AMPK and MEK/ERK1/2 reversed the effect of baicalein on RUNX3 and FOXO3a protein expression. baicalein 71-80 RUNX family transcription factor 3 Homo sapiens 84-89 25948105-14 2015 On the contrary, overexpression of FOXO3a restored the effect of baicalein on cell growth inhibition in cells silencing of endogenous FOXO3a gene and enhanced the effect of baicalein on RUNX3 protein expression. baicalein 173-182 RUNX family transcription factor 3 Homo sapiens 186-191 25948105-16 2015 CONCLUSION: Collectively, our results show that baicalein inhibits growth and induces apoptosis of NSCLC cells through AMPKalpha- and MEK/ERK1/2-mediated increase and interaction of FOXO3a and RUNX3 protein. baicalein 48-57 RUNX family transcription factor 3 Homo sapiens 193-198 25948105-18 2015 This study reveals a novel mechanism for regulating FOXO3a and RUNX3 signaling axis in response to baicalein and suggests a new strategy for NSCLC associated targeted therapy. baicalein 99-108 RUNX family transcription factor 3 Homo sapiens 63-68 25612675-7 2015 In support of a functional role, hypermethylation of RUNX3 was correlated with low levels of protein, and treatment of cell lines with the DNA demethylating agent, decitabine, resulted in mRNA re-expression. Decitabine 164-174 RUNX family transcription factor 3 Homo sapiens 53-58 25975905-3 2015 Immunohistochemical SP method was used to detect the expression of ER and Runx3 proteins in 113 tissue samples of breast cancer. TFF2 protein, human 20-22 RUNX family transcription factor 3 Homo sapiens 74-79 25811792-2 2015 Described here are the synthesis, biological evaluation, and pharmacokinetic evaluation of new synthetic small molecules based on pyridone-based HDAC inhibitors that specifically stabilize RUNX3 by acetylation and regulate its function. Pyridones 130-138 RUNX family transcription factor 3 Homo sapiens 189-194 25811792-4 2015 Notably, one of these new derivatives, (E)-N-hydroxy-3-(2-oxo-1-(quinolin-2-ylmethyl)-1,2-dihydropyridin-3-yl)acrylamide (4l), significantly restored RUNX3 in a dose-dependent manner and showed high metabolic stability, a good pharmacokinetic profile with high oral bioavailability and long half-life, and strong antitumor activity. (e)-n-hydroxy-3-(2-oxo-1-(quinolin-2-ylmethyl)-1,2-dihydropyridin-3-yl)acrylamide 39-120 RUNX family transcription factor 3 Homo sapiens 150-155 25811792-5 2015 This study suggests that pyridone-based analogues modulate RUNX3 activity through epigenetic regulation as well as strong transcriptional and post-translational regulation of RUNX3 and could be potential clinical candidates as orally available RUNX3 modulators for the treatment of cancer. Pyridones 25-33 RUNX family transcription factor 3 Homo sapiens 59-64 25811792-5 2015 This study suggests that pyridone-based analogues modulate RUNX3 activity through epigenetic regulation as well as strong transcriptional and post-translational regulation of RUNX3 and could be potential clinical candidates as orally available RUNX3 modulators for the treatment of cancer. Pyridones 25-33 RUNX family transcription factor 3 Homo sapiens 175-180 25811792-5 2015 This study suggests that pyridone-based analogues modulate RUNX3 activity through epigenetic regulation as well as strong transcriptional and post-translational regulation of RUNX3 and could be potential clinical candidates as orally available RUNX3 modulators for the treatment of cancer. Pyridones 25-33 RUNX family transcription factor 3 Homo sapiens 175-180 26225676-0 2015 Increased Oxidative Stress and RUNX3 Hypermethylation in Patients with Hepatitis B Virus-Associated Hepatocellular Carcinoma (HCC) and Induction of RUNX3 Hypermethylation by Reactive Oxygen Species in HCC Cells. Reactive Oxygen Species 174-197 RUNX family transcription factor 3 Homo sapiens 148-153 25784989-4 2015 Herein, using BSP to assess the 5 mC level in promoters of ten specific marker gene in PCa, our results present that Cdh1, Gstp1, Pten, Apc, Runx3 and Mgmt are observed to be hypermethylated in promoters and lower expression while Cyr61, Sema3c and Ptgs2 are reversed patterns compared to the normal prostate tissues. Methylcholanthrene 34-36 RUNX family transcription factor 3 Homo sapiens 141-146 23700080-0 2015 RUNX3 confers sensitivity to pheophorbide a-photodynamic therapy in human oral squamous cell carcinoma cell lines. pheophorbide a 29-43 RUNX family transcription factor 3 Homo sapiens 0-5 23700080-10 2015 We found that the cytotoxicity by Pa-PDT was proportional to RUNX3 expression in OSCC cell lines. pheophorbide a 34-36 RUNX family transcription factor 3 Homo sapiens 61-66 23700080-11 2015 Additionally, knockdown of RUNX3 expression reduced cytotoxicity by Pa-PDT, suggesting that RUNX3 might be a biomarker to determine sensitivity to Pa-PDT. pheophorbide a 68-70 RUNX family transcription factor 3 Homo sapiens 27-32 23700080-11 2015 Additionally, knockdown of RUNX3 expression reduced cytotoxicity by Pa-PDT, suggesting that RUNX3 might be a biomarker to determine sensitivity to Pa-PDT. pheophorbide a 68-70 RUNX family transcription factor 3 Homo sapiens 92-97 23700080-11 2015 Additionally, knockdown of RUNX3 expression reduced cytotoxicity by Pa-PDT, suggesting that RUNX3 might be a biomarker to determine sensitivity to Pa-PDT. pheophorbide a 147-149 RUNX family transcription factor 3 Homo sapiens 27-32 23700080-11 2015 Additionally, knockdown of RUNX3 expression reduced cytotoxicity by Pa-PDT, suggesting that RUNX3 might be a biomarker to determine sensitivity to Pa-PDT. pheophorbide a 147-149 RUNX family transcription factor 3 Homo sapiens 92-97 26225676-6 2015 Effect of reactive oxygen species (ROS) on induction of RUNX3 hypermethylation in HCC cells was investigated. Reactive Oxygen Species 10-33 RUNX family transcription factor 3 Homo sapiens 56-61 26225676-6 2015 Effect of reactive oxygen species (ROS) on induction of RUNX3 hypermethylation in HCC cells was investigated. Reactive Oxygen Species 35-38 RUNX family transcription factor 3 Homo sapiens 56-61 26225676-10 2015 RUNX3 methylation in hydrogen peroxide (H2O2)-treated HepG2 cells was significantly higher than in untreated control cells. Hydrogen Peroxide 21-38 RUNX family transcription factor 3 Homo sapiens 0-5 26225676-10 2015 RUNX3 methylation in hydrogen peroxide (H2O2)-treated HepG2 cells was significantly higher than in untreated control cells. Hydrogen Peroxide 40-44 RUNX family transcription factor 3 Homo sapiens 0-5 26225676-14 2015 In vitro, RUNX3 hypermethylation was experimentally induced by H2O2. Hydrogen Peroxide 63-67 RUNX family transcription factor 3 Homo sapiens 10-15 24957188-0 2015 RUNX3 expression is associated with sensitivity to pheophorbide a-based photodynamic therapy in keloids. pheophorbide a 51-65 RUNX family transcription factor 3 Homo sapiens 0-5 24957188-2 2015 In this study, we aimed to elucidate the implications of RUNX3 for keloid pathogenesis and sensitivity to pheophorbide a-based PDT (Pa-PDT). pheophorbide a 106-120 RUNX family transcription factor 3 Homo sapiens 57-62 24957188-8 2015 In addition, RUNX3 expression was significantly decreased after Pa-PDT in KFs, and KFs with downregulation of RUNX3 showed significantly increased cell viability after Pa-PDT. Protactinium 64-66 RUNX family transcription factor 3 Homo sapiens 13-18 24957188-8 2015 In addition, RUNX3 expression was significantly decreased after Pa-PDT in KFs, and KFs with downregulation of RUNX3 showed significantly increased cell viability after Pa-PDT. Protactinium 168-170 RUNX family transcription factor 3 Homo sapiens 110-115 25066130-5 2014 Indeed, Runx1;Runx3 DKO cells showed mitomycin C hypersensitivity, due to impairment of monoubiquitinated-FANCD2 recruitment to DNA damage foci, although FANCD2 monoubiquitination in the FA pathway was unaffected. Mitomycin 37-48 RUNX family transcription factor 3 Homo sapiens 14-19 25333219-5 2014 The percentage of RUNX3 methylation and negative RUNX3 protein expression in the eutopic endometrium from the EAOC group was significantly higher than that in the EM and CE groups. eaoc 110-114 RUNX family transcription factor 3 Homo sapiens 18-23 25333219-5 2014 The percentage of RUNX3 methylation and negative RUNX3 protein expression in the eutopic endometrium from the EAOC group was significantly higher than that in the EM and CE groups. eaoc 110-114 RUNX family transcription factor 3 Homo sapiens 49-54 24812032-10 2014 Stable suppression of RUNX3 expression in the Ewing sarcoma cell line A673 delayed colony growth in anchorage independent soft agar assays and reversed expression of EWS/FLI-responsive genes. Agar 127-131 RUNX family transcription factor 3 Homo sapiens 22-27 24535051-0 2014 Effects of 5-azacytidine on RUNX3 gene expression and the biological behavior of esophageal carcinoma cells. Azacitidine 11-24 RUNX family transcription factor 3 Homo sapiens 28-33 24748977-0 2014 CpG-oligodeoxynucleotides suppress the proliferation of A549 lung adenocarcinoma cells via toll-like receptor 9 signaling and upregulation of Runt-related transcription factor 3 expression. CPG-oligonucleotide 0-25 RUNX family transcription factor 3 Homo sapiens 142-177 24748977-3 2014 Moreover, Runx3 siRNA was synthesized and transiently transfected into the A549 cells and the MTT assay was used to detect the effects of CpG-ODN on transfected cell growth. monooxyethylene trimethylolpropane tristearate 94-97 RUNX family transcription factor 3 Homo sapiens 10-15 24748977-3 2014 Moreover, Runx3 siRNA was synthesized and transiently transfected into the A549 cells and the MTT assay was used to detect the effects of CpG-ODN on transfected cell growth. cpg-odn 138-145 RUNX family transcription factor 3 Homo sapiens 10-15 24535051-1 2014 The present study investigated the effects of 5-azacytidine (5-azaC) on the expression level of the human runt-related transcription factor 3 (RUNX3) gene and the biological behavior of esophageal carcinoma Eca109 cells. Azacitidine 46-59 RUNX family transcription factor 3 Homo sapiens 106-141 24535051-1 2014 The present study investigated the effects of 5-azacytidine (5-azaC) on the expression level of the human runt-related transcription factor 3 (RUNX3) gene and the biological behavior of esophageal carcinoma Eca109 cells. Azacitidine 46-59 RUNX family transcription factor 3 Homo sapiens 143-148 24535051-1 2014 The present study investigated the effects of 5-azacytidine (5-azaC) on the expression level of the human runt-related transcription factor 3 (RUNX3) gene and the biological behavior of esophageal carcinoma Eca109 cells. Azacitidine 61-67 RUNX family transcription factor 3 Homo sapiens 106-141 24535051-1 2014 The present study investigated the effects of 5-azacytidine (5-azaC) on the expression level of the human runt-related transcription factor 3 (RUNX3) gene and the biological behavior of esophageal carcinoma Eca109 cells. Azacitidine 61-67 RUNX family transcription factor 3 Homo sapiens 143-148 24535051-4 2014 When treated with 5-azaC at hypoxic levels, the expression of RUNX3 increased and the methylation degree of the RUNX3 gene was decreased significantly in Eca109 cells. Azacitidine 18-24 RUNX family transcription factor 3 Homo sapiens 62-67 24535051-4 2014 When treated with 5-azaC at hypoxic levels, the expression of RUNX3 increased and the methylation degree of the RUNX3 gene was decreased significantly in Eca109 cells. Azacitidine 18-24 RUNX family transcription factor 3 Homo sapiens 112-117 24535051-5 2014 5-azaC at 50 microM demonstrated the highest RUNX3-induction activity, inducing RUNX3 mRNA and protein expression, and decreasing the degree of methylation of the RUNX3 gene. Azacitidine 0-6 RUNX family transcription factor 3 Homo sapiens 45-50 24535051-5 2014 5-azaC at 50 microM demonstrated the highest RUNX3-induction activity, inducing RUNX3 mRNA and protein expression, and decreasing the degree of methylation of the RUNX3 gene. Azacitidine 0-6 RUNX family transcription factor 3 Homo sapiens 80-85 24535051-5 2014 5-azaC at 50 microM demonstrated the highest RUNX3-induction activity, inducing RUNX3 mRNA and protein expression, and decreasing the degree of methylation of the RUNX3 gene. Azacitidine 0-6 RUNX family transcription factor 3 Homo sapiens 80-85 24535051-6 2014 Methylation specific PCR indicated that 5-azaC induced RUNX3 expression through demethylation. Azacitidine 40-46 RUNX family transcription factor 3 Homo sapiens 55-60 24535051-10 2014 Taken together, our findings demonstrated that the RUNX3 gene is hypermethylated in Eca109 cells and that 5-azaC induces the expression of the RUNX3 gene by demethylation, which inhibits the proliferation, migration and invasion of Eca109 cells. Azacitidine 106-112 RUNX family transcription factor 3 Homo sapiens 143-148 23892093-0 2013 Epigenetic downregulation of RUNX3 by DNA methylation induces docetaxel chemoresistance in human lung adenocarcinoma cells by activation of the AKT pathway. Docetaxel 62-71 RUNX family transcription factor 3 Homo sapiens 29-34 24376239-0 2014 Lactam-based HDAC inhibitors for anticancer chemotherapy: restoration of RUNX3 by posttranslational modification and epigenetic control. Lactams 0-6 RUNX family transcription factor 3 Homo sapiens 73-78 24376239-4 2014 Thus, lactam-based HDAC inhibitors were screened to identify potent protein stabilizers that maintain RUNX3 stability by acetylation. Lactams 6-12 RUNX family transcription factor 3 Homo sapiens 102-107 24376239-6 2014 3-[1-(4-Bromobenzyl)-2-oxo-2,5-dihydro-1H-pyrrol-3-yl]-N-hydroxypropanamide (11-8) significantly increased RUNX3 acetylation and stability with relatively low RUNX3 mRNA expression and HDAC inhibitory activity. 3-[1-(4-bromobenzyl)-2-oxo-2,5-dihydro-1h-pyrrol-3-yl]-n-hydroxypropanamide 0-75 RUNX family transcription factor 3 Homo sapiens 107-112 24376239-6 2014 3-[1-(4-Bromobenzyl)-2-oxo-2,5-dihydro-1H-pyrrol-3-yl]-N-hydroxypropanamide (11-8) significantly increased RUNX3 acetylation and stability with relatively low RUNX3 mRNA expression and HDAC inhibitory activity. 3-[1-(4-bromobenzyl)-2-oxo-2,5-dihydro-1h-pyrrol-3-yl]-n-hydroxypropanamide 0-75 RUNX family transcription factor 3 Homo sapiens 159-164 24100442-3 2013 Compound K treatment induced unmethylation of the RUNX3 promoter region such as TSA treatment and an accumulation of acetylated histones H3 and H4 within the total cellular chromatin, resulting in an enhanced ability of these histones to bind to the promoter sequences of the tumor suppressor gene Runt-related transcription factor 3 (RUNX3). trichostatin A 80-83 RUNX family transcription factor 3 Homo sapiens 50-55 23542169-7 2014 In addition, RUNX3 directly interacted with the C-terminal activation domain of HIF-1alpha and prolyl hydroxylase (PHD) 2 and enhanced the interaction between HIF-1alpha and PHD2, which potentiated proline hydroxylation and promoted the degradation of HIF-1alpha. Proline 198-205 RUNX family transcription factor 3 Homo sapiens 13-18 23542169-9 2014 Taken together, these results suggest that RUNX3 destabilizes HIF-1alpha protein by promoting the proline hydroxylation of HIF-1alpha through binding to HIF-1alpha/PHD2. Proline 98-105 RUNX family transcription factor 3 Homo sapiens 43-48 24403453-0 2014 Demethylation of RUNX3 by vincristine in colorectal adenocarcinoma cells. Vincristine 26-37 RUNX family transcription factor 3 Homo sapiens 17-22 24403453-7 2014 RESULTS: RUNX3 was demethylated after vincristine treatment in DLD-1 cells. Vincristine 38-49 RUNX family transcription factor 3 Homo sapiens 9-14 24403453-8 2014 The expression of RUNX3 mRNA was down-regulated in DLD-1 cells because of DNA hypermethylation, but was restored after vincristine treatment. Vincristine 119-130 RUNX family transcription factor 3 Homo sapiens 18-23 24403453-12 2014 CONCLUSION: These results demonstrate that vincristine demethylates RUNX3 in colorectal adenocarcinoma cells, and restores its expression. Vincristine 43-54 RUNX family transcription factor 3 Homo sapiens 68-73 23892093-8 2013 Immunohistochemical analysis revealed that decreased RUNX3 expression was correlated with high expression of Akt1 and decreased sensitivity of patients to docetaxel-based chemotherapy. Docetaxel 155-164 RUNX family transcription factor 3 Homo sapiens 53-58 23892093-9 2013 Taken together, our results suggest that epigenetic downregulation of RUNX3 can induce docetaxel resistance in human lung adenocarcinoma cells by activating AKT signaling and increasing expression of RUNX3 may represent a promising strategy for reversing docetaxel resistance in the future. Docetaxel 87-96 RUNX family transcription factor 3 Homo sapiens 70-75 23892093-9 2013 Taken together, our results suggest that epigenetic downregulation of RUNX3 can induce docetaxel resistance in human lung adenocarcinoma cells by activating AKT signaling and increasing expression of RUNX3 may represent a promising strategy for reversing docetaxel resistance in the future. Docetaxel 87-96 RUNX family transcription factor 3 Homo sapiens 200-205 23892093-2 2013 Here, we investigated the effect of epigenetic downregulation of RUNX3 in docetaxel resistance of human lung adenocarcinoma and its possible molecular mechanisms. Docetaxel 74-83 RUNX family transcription factor 3 Homo sapiens 65-70 23892093-9 2013 Taken together, our results suggest that epigenetic downregulation of RUNX3 can induce docetaxel resistance in human lung adenocarcinoma cells by activating AKT signaling and increasing expression of RUNX3 may represent a promising strategy for reversing docetaxel resistance in the future. Docetaxel 255-264 RUNX family transcription factor 3 Homo sapiens 70-75 23892093-3 2013 RUNX3 was found to be downregulated by hypermethylation in docetaxel-resistant lung adenocarcinoma cells. Docetaxel 59-68 RUNX family transcription factor 3 Homo sapiens 0-5 23892093-9 2013 Taken together, our results suggest that epigenetic downregulation of RUNX3 can induce docetaxel resistance in human lung adenocarcinoma cells by activating AKT signaling and increasing expression of RUNX3 may represent a promising strategy for reversing docetaxel resistance in the future. Docetaxel 255-264 RUNX family transcription factor 3 Homo sapiens 200-205 23892093-5 2013 Conversely, knockdown of RUNX3 could lead to the decreased sensitivity of parental human lung adenocarcinoma cells to docetaxel by enhancing proliferative capacity. Docetaxel 118-127 RUNX family transcription factor 3 Homo sapiens 25-30 23892093-6 2013 Furthermore, we showed that overexpression of RUNX3 could inactivate the AKT/GSK3beta/beta-catenin signaling pathway in the docetaxel-resistant cells. Docetaxel 124-133 RUNX family transcription factor 3 Homo sapiens 46-51 23892093-7 2013 Importantly, co-transfection of RUNX3 and constitutively active Akt1 could reverse the effects of RUNX3 overexpression, while treatment with the MK-2206 (AKT inhibitor) mimicked the effects of RUNX3 overexpression in docetaxel-resistant human lung adenocarcinoma cells. Docetaxel 217-226 RUNX family transcription factor 3 Homo sapiens 32-37 23723708-2 2013 The aim of this study was to investigate the effects of 5-aza-2"-deoxycytidine (5-Aza-CdR) on cell proliferation and apoptosis by demethylation of the promoter region and restoring the expression of RUNX3 in the breast cancer MCF-7 cell line. Decitabine 56-78 RUNX family transcription factor 3 Homo sapiens 199-204 23504038-0 2013 Effects of paeonol on intracellular calcium concentration and expression of RUNX3 in LoVo human colon cancer cells. paeonol 11-18 RUNX family transcription factor 3 Homo sapiens 76-81 23504038-7 2013 Furthermore, RUNX3 gene expression was increased in paeonol-treated cells. paeonol 52-59 RUNX family transcription factor 3 Homo sapiens 13-18 23504038-9 2013 One of the antitumor mechanisms of paeonol may be its apoptosis-inducing activity through an increased intracellular calcium concentration and the upregulation of RUNX3 expression. paeonol 35-42 RUNX family transcription factor 3 Homo sapiens 163-168 24042352-5 2013 The levels of RUNX3 mRNA and protein were downregulated in response to treatment of the human colorectal cancer cell line SNU-407 with H2O2. Hydrogen Peroxide 135-139 RUNX family transcription factor 3 Homo sapiens 14-19 24042352-6 2013 Treatment of the cells with H2O2 also upregulated Akt mRNA and protein expression, and inhibited the binding of RUNX3 to the Akt promoter. Hydrogen Peroxide 28-32 RUNX family transcription factor 3 Homo sapiens 112-117 24042352-7 2013 The inverse correlation between the expression levels of RUNX3 and Akt in H2O2-treated cells was also associated with nuclear translocation of beta-catenin and upregulation of cyclin D1 expression, which induced cell proliferation. Hydrogen Peroxide 74-78 RUNX family transcription factor 3 Homo sapiens 57-62 24042352-9 2013 The results presented here demonstrate that reactive oxygen species silence the tumor suppressor RUNX3, enhance the Akt-mediated signaling pathway, and promote the proliferation of colorectal cancer cells. Reactive Oxygen Species 44-67 RUNX family transcription factor 3 Homo sapiens 97-102 23664167-0 2013 Loss of runt-related transcription factor 3 induces gemcitabine resistance in pancreatic cancer. gemcitabine 52-63 RUNX family transcription factor 3 Homo sapiens 8-43 23664167-11 2013 Exogenous RUNX3 expression decreased gemcitabine IC50 in RUNX3-negative cells. gemcitabine 37-48 RUNX family transcription factor 3 Homo sapiens 10-15 23664167-11 2013 Exogenous RUNX3 expression decreased gemcitabine IC50 in RUNX3-negative cells. gemcitabine 37-48 RUNX family transcription factor 3 Homo sapiens 57-62 23664167-12 2013 CONCLUSION: Loss of RUNX3 expression contributes to gemcitabine resistance by inducing MRP expression, thereby resulting in poor patient survival. gemcitabine 52-63 RUNX family transcription factor 3 Homo sapiens 20-25 22580604-6 2013 In addition, Pin1 recognizes four phosphorylated Ser/Thr-Pro motifs in RUNX3 via its WW domain. Serine 49-52 RUNX family transcription factor 3 Homo sapiens 71-76 23549984-7 2013 After treatment of human gastric cancer AGS and BGC-823 cells with the DNA methylation inhibitor 5-aza-2"-deoxycytidine, a significant increase in RUNX3 mRNA, RUNX3 protein, and the non-methylated form of the RUNX3 promoter were observed relative to untreated cells. Decitabine 97-119 RUNX family transcription factor 3 Homo sapiens 147-152 23549984-7 2013 After treatment of human gastric cancer AGS and BGC-823 cells with the DNA methylation inhibitor 5-aza-2"-deoxycytidine, a significant increase in RUNX3 mRNA, RUNX3 protein, and the non-methylated form of the RUNX3 promoter were observed relative to untreated cells. Decitabine 97-119 RUNX family transcription factor 3 Homo sapiens 159-164 23549984-7 2013 After treatment of human gastric cancer AGS and BGC-823 cells with the DNA methylation inhibitor 5-aza-2"-deoxycytidine, a significant increase in RUNX3 mRNA, RUNX3 protein, and the non-methylated form of the RUNX3 promoter were observed relative to untreated cells. Decitabine 97-119 RUNX family transcription factor 3 Homo sapiens 159-164 22580604-6 2013 In addition, Pin1 recognizes four phosphorylated Ser/Thr-Pro motifs in RUNX3 via its WW domain. Threonine 53-56 RUNX family transcription factor 3 Homo sapiens 71-76 22580604-6 2013 In addition, Pin1 recognizes four phosphorylated Ser/Thr-Pro motifs in RUNX3 via its WW domain. Proline 57-60 RUNX family transcription factor 3 Homo sapiens 71-76 24175838-0 2013 Alteration of runt-related transcription factor 3 gene expression and biologic behavior of esophageal carcinoma TE-1 cells after 5-azacytidine intervention. Azacitidine 129-142 RUNX family transcription factor 3 Homo sapiens 14-49 23555166-14 2013 High intakes of carbohydrate, vitamin B1, and vitamin E may decrease the risk of RUNX3 methylation in gastric cancer tissue, particularly in CagA- or H. pylori-negative infection, with OR of 0.41 (0.19-0.90), 0.42 (0.20-0.89), and 0.29 (0.13-0.62), respectively. Carbohydrates 16-28 RUNX family transcription factor 3 Homo sapiens 81-86 23555166-14 2013 High intakes of carbohydrate, vitamin B1, and vitamin E may decrease the risk of RUNX3 methylation in gastric cancer tissue, particularly in CagA- or H. pylori-negative infection, with OR of 0.41 (0.19-0.90), 0.42 (0.20-0.89), and 0.29 (0.13-0.62), respectively. Thiamine 30-40 RUNX family transcription factor 3 Homo sapiens 81-86 23555166-14 2013 High intakes of carbohydrate, vitamin B1, and vitamin E may decrease the risk of RUNX3 methylation in gastric cancer tissue, particularly in CagA- or H. pylori-negative infection, with OR of 0.41 (0.19-0.90), 0.42 (0.20-0.89), and 0.29 (0.13-0.62), respectively. Vitamin E 46-55 RUNX family transcription factor 3 Homo sapiens 81-86 24175838-6 2013 The expression level of RUNX3 mRNA increased significantly in TE-1 cells after treatment with 5-azaC at hypotoxic levels. Azacitidine 94-100 RUNX family transcription factor 3 Homo sapiens 24-29 24175838-7 2013 RT-PCR showed 5-azaC at 50 muM had the highest RUNX3-induction activity. Azacitidine 14-20 RUNX family transcription factor 3 Homo sapiens 47-52 24175838-8 2013 Methylation-specific PCR indicated that 5-azaC induced RUNX3 expression through demethylation. Azacitidine 40-46 RUNX family transcription factor 3 Homo sapiens 55-60 23886181-5 2013 Methylation levels of LINE-1 and RUNX3 promoter were measured by combined bisulfite restriction analysis PCR and methylation-specific PCR, respectively. hydrogen sulfite 74-83 RUNX family transcription factor 3 Homo sapiens 33-38 24175838-10 2013 In conclusion, we demonstrate that the RUNX3 gene can be reactivated by the demethylation reagent 5-azaC, which inhibits the proliferation, migration and invasion of esophageal carcinoma TE-1 cells. Azacitidine 98-104 RUNX family transcription factor 3 Homo sapiens 39-44 23886181-7 2013 Methylation of RUNX3 promoter was significantly increased in cells exposed to H2O2. Hydrogen Peroxide 78-82 RUNX family transcription factor 3 Homo sapiens 15-20 23886181-9 2013 In conclusion, hypomethylation of LINE-1 and hypermethylation of RUNX3 promoter in bladder cancer cell line was experimentally induced by reactive oxygen species (ROS). Reactive Oxygen Species 138-161 RUNX family transcription factor 3 Homo sapiens 65-70 22179198-2 2012 The aim of this study was to assess whether 5-aza-CdR and TSA inhibit the growth of leukaemia cells and induce caspase-3-dependent apoptosis by upregulating RUNX3 expression. trichostatin A 58-61 RUNX family transcription factor 3 Homo sapiens 157-162 23886181-9 2013 In conclusion, hypomethylation of LINE-1 and hypermethylation of RUNX3 promoter in bladder cancer cell line was experimentally induced by reactive oxygen species (ROS). Reactive Oxygen Species 163-166 RUNX family transcription factor 3 Homo sapiens 65-70 23648294-0 2013 [Effect of 5-aza-2"-deoxycytidine on growth and methylation of RUNX3 gene in human pancreatic cancer cell line MiaPaca2]. Decitabine 11-33 RUNX family transcription factor 3 Homo sapiens 63-68 23648294-1 2013 OBJECTIVE: To investigate the effect of demethylating agent 5-aza-2"-deoxycytidine (5-Aza-CdR) on the growth of human pancreatic cancer cell line MiaPaca2 and the expression and methylation of tumor suppressor gene RUNX3. Decitabine 60-82 RUNX family transcription factor 3 Homo sapiens 215-220 22413885-5 2012 RESULTS: Calcium-dependent activation of T cells using CD3/CD28 and PMA/CD3 stimulation induced a Th1 expression profile reflected by increased expression of T-bet, RUNX3, IL-2, and IFNgamma, whereas calcium-independent activation via PMA/CD28 induced a Th2 expression profile which included GATA3, RXRA, CCL1 and Itk. Calcium 9-16 RUNX family transcription factor 3 Homo sapiens 165-170 22179198-0 2012 RUNX3 is involved in caspase-3-dependent apoptosis induced by a combination of 5-aza-CdR and TSA in leukaemia cell lines. trichostatin A 93-96 RUNX family transcription factor 3 Homo sapiens 0-5 23269881-3 2012 Additionally, using reverse transcriptase-polymerase chain reaction, we analyzed RUNX3 gene expression in several thyroid cancer cell lines after treating with the demethylating agent 5-aza-2"-deoxycytidine (DAC). Decitabine 184-206 RUNX family transcription factor 3 Homo sapiens 81-86 23269881-3 2012 Additionally, using reverse transcriptase-polymerase chain reaction, we analyzed RUNX3 gene expression in several thyroid cancer cell lines after treating with the demethylating agent 5-aza-2"-deoxycytidine (DAC). Decitabine 208-211 RUNX family transcription factor 3 Homo sapiens 81-86 22846564-0 2012 Upregulated miR-130a increases drug resistance by regulating RUNX3 and Wnt signaling in cisplatin-treated HCC cell. Cisplatin 88-97 RUNX family transcription factor 3 Homo sapiens 61-66 21791485-7 2012 The promoter regions of subset of genes highly specific to characterize the CIMP status (NEUROG1, IGF2, RUNX3, SOCS1, including MLH1) were hypermethylated, suggesting the presence of CIMP+ and MSI high tumor. Cyclic IMP 76-80 RUNX family transcription factor 3 Homo sapiens 104-109 22274925-2 2012 This study investigated the mechanisms involved in reactive oxygen species (ROS)-induced silencing of RUNX3 in terms of epigenetic alteration since the effects of oxidative stress in tumor suppressor gene transcription are largely unknown. Reactive Oxygen Species 51-74 RUNX family transcription factor 3 Homo sapiens 102-107 22274925-2 2012 This study investigated the mechanisms involved in reactive oxygen species (ROS)-induced silencing of RUNX3 in terms of epigenetic alteration since the effects of oxidative stress in tumor suppressor gene transcription are largely unknown. Reactive Oxygen Species 76-79 RUNX family transcription factor 3 Homo sapiens 102-107 22274925-3 2012 RUNX3 mRNA and protein expressions were down-regulated in response to hydrogen peroxide (H(2)O(2)) in the human colorectal cancer cell line SNU-407. Hydrogen Peroxide 70-87 RUNX family transcription factor 3 Homo sapiens 0-5 22274925-5 2012 Moreover, methylation-specific PCR data revealed that H(2)O(2) treatment increased RUNX3 promoter methylation; however, NAC and the cytosine methylation inhibitor, 5-aza-2-deoxycytidine (5-Aza-dC), decreased it, suggesting that an epigenetic regulatory mechanism by ROS-induced methylation may be involved in RUNX3 silencing. Hydrogen Peroxide 54-62 RUNX family transcription factor 3 Homo sapiens 83-88 22274925-5 2012 Moreover, methylation-specific PCR data revealed that H(2)O(2) treatment increased RUNX3 promoter methylation; however, NAC and the cytosine methylation inhibitor, 5-aza-2-deoxycytidine (5-Aza-dC), decreased it, suggesting that an epigenetic regulatory mechanism by ROS-induced methylation may be involved in RUNX3 silencing. Hydrogen Peroxide 54-62 RUNX family transcription factor 3 Homo sapiens 309-314 22274925-5 2012 Moreover, methylation-specific PCR data revealed that H(2)O(2) treatment increased RUNX3 promoter methylation; however, NAC and the cytosine methylation inhibitor, 5-aza-2-deoxycytidine (5-Aza-dC), decreased it, suggesting that an epigenetic regulatory mechanism by ROS-induced methylation may be involved in RUNX3 silencing. Decitabine 164-185 RUNX family transcription factor 3 Homo sapiens 309-314 22274925-5 2012 Moreover, methylation-specific PCR data revealed that H(2)O(2) treatment increased RUNX3 promoter methylation; however, NAC and the cytosine methylation inhibitor, 5-aza-2-deoxycytidine (5-Aza-dC), decreased it, suggesting that an epigenetic regulatory mechanism by ROS-induced methylation may be involved in RUNX3 silencing. Decitabine 187-195 RUNX family transcription factor 3 Homo sapiens 83-88 22274925-5 2012 Moreover, methylation-specific PCR data revealed that H(2)O(2) treatment increased RUNX3 promoter methylation; however, NAC and the cytosine methylation inhibitor, 5-aza-2-deoxycytidine (5-Aza-dC), decreased it, suggesting that an epigenetic regulatory mechanism by ROS-induced methylation may be involved in RUNX3 silencing. Reactive Oxygen Species 266-269 RUNX family transcription factor 3 Homo sapiens 83-88 22274925-7 2012 In addition, 5-Aza-dC treatment prevented the decrease in RUNX3 mRNA and protein levels by H(2)O(2) treatment. Azacitidine 13-18 RUNX family transcription factor 3 Homo sapiens 58-63 22274925-8 2012 Additionally, H(2)O(2) treatment inhibited the nuclear localization and expression of RUNX3, which was abolished by NAC treatment. Hydrogen Peroxide 14-22 RUNX family transcription factor 3 Homo sapiens 86-91 22274925-8 2012 Additionally, H(2)O(2) treatment inhibited the nuclear localization and expression of RUNX3, which was abolished by NAC treatment. Acetylcysteine 116-119 RUNX family transcription factor 3 Homo sapiens 86-91 22274925-10 2012 Taken together, the data suggested that ROS silenced the tumor suppressor, RUNX3, by epigenetic regulation and may therefore be associated with the progression of colorectal cancer. Reactive Oxygen Species 40-43 RUNX family transcription factor 3 Homo sapiens 75-80 22076387-14 2012 In in vitro experiments, exogenous expression of RUNX3 strongly inhibited cell growth in GCTB by MTT (P<0.05), induced apoptosis as evidenced by Annexin V-FITC and increased G1 phase ratio by PI (P<0.05). monooxyethylene trimethylolpropane tristearate 109-112 RUNX family transcription factor 3 Homo sapiens 49-54 22179198-8 2012 Demethylating drug 5-aza-CdR could induce RUNX3 expression, but the combination of TSA and 5-aza-CdR had a greater effect than did treatment with a single compound. trichostatin A 83-86 RUNX family transcription factor 3 Homo sapiens 42-47 22179198-9 2012 The combination of 5-aza-CdR and TSA induced the translocation of RUNX3 from the cytoplasm into the nucleus. trichostatin A 33-36 RUNX family transcription factor 3 Homo sapiens 66-71 22179198-13 2012 CONCLUSION: RUNX3 plays an important role in leukaemia cellular functions, and the induction of RUNX3-mediated effects may contribute to the therapeutic value of combination TSA and 5-aza-CdR treatment. trichostatin A 174-177 RUNX family transcription factor 3 Homo sapiens 96-101 21658745-1 2011 We investigated the spreading pattern of runt-related transcription factor-3 (RUNX3) C-phosphate-G (CpG) island (3478 base pairs) methylation in salivary gland adenoid cystic carcinoma. Phosphates 87-96 RUNX family transcription factor 3 Homo sapiens 41-76 21968610-2 2012 Down-regulated CAT expression in AML-2/DX100 cells was completely recovered after treatment of hydrogen peroxide (H(2)O(2)) and histone deacetylase inhibitor, trichostatin A (TSA) but was increased slightly by the treatment of DNA methylation inhibitor, 5-aza-2"-deoxycytidine (5-AdC). Hydrogen Peroxide 95-112 RUNX family transcription factor 3 Homo sapiens 33-38 21968610-2 2012 Down-regulated CAT expression in AML-2/DX100 cells was completely recovered after treatment of hydrogen peroxide (H(2)O(2)) and histone deacetylase inhibitor, trichostatin A (TSA) but was increased slightly by the treatment of DNA methylation inhibitor, 5-aza-2"-deoxycytidine (5-AdC). Hydrogen Peroxide 114-122 RUNX family transcription factor 3 Homo sapiens 33-38 21968610-2 2012 Down-regulated CAT expression in AML-2/DX100 cells was completely recovered after treatment of hydrogen peroxide (H(2)O(2)) and histone deacetylase inhibitor, trichostatin A (TSA) but was increased slightly by the treatment of DNA methylation inhibitor, 5-aza-2"-deoxycytidine (5-AdC). trichostatin A 159-173 RUNX family transcription factor 3 Homo sapiens 33-38 21968610-2 2012 Down-regulated CAT expression in AML-2/DX100 cells was completely recovered after treatment of hydrogen peroxide (H(2)O(2)) and histone deacetylase inhibitor, trichostatin A (TSA) but was increased slightly by the treatment of DNA methylation inhibitor, 5-aza-2"-deoxycytidine (5-AdC). trichostatin A 175-178 RUNX family transcription factor 3 Homo sapiens 33-38 21968610-2 2012 Down-regulated CAT expression in AML-2/DX100 cells was completely recovered after treatment of hydrogen peroxide (H(2)O(2)) and histone deacetylase inhibitor, trichostatin A (TSA) but was increased slightly by the treatment of DNA methylation inhibitor, 5-aza-2"-deoxycytidine (5-AdC). Decitabine 254-276 RUNX family transcription factor 3 Homo sapiens 33-38 21968610-2 2012 Down-regulated CAT expression in AML-2/DX100 cells was completely recovered after treatment of hydrogen peroxide (H(2)O(2)) and histone deacetylase inhibitor, trichostatin A (TSA) but was increased slightly by the treatment of DNA methylation inhibitor, 5-aza-2"-deoxycytidine (5-AdC). Decitabine 278-283 RUNX family transcription factor 3 Homo sapiens 33-38 21968610-5 2012 Meanwhile, overexpression of other up-regulated peroxidase genes appears to make compensation for decreased H(2)O(2)-scavenging activity for the down-regulated CAT expression in AML-2/DX100 cells. Hydrogen Peroxide 108-116 RUNX family transcription factor 3 Homo sapiens 178-183 23243425-0 2012 Downregulation of Hlx closely related to the decreased expressions of T-bet and Runx3 in patients with gastric cancer may be associated with a pathological event leading to the imbalance of Th1/Th2. hlx 18-21 RUNX family transcription factor 3 Homo sapiens 80-85 21658745-1 2011 We investigated the spreading pattern of runt-related transcription factor-3 (RUNX3) C-phosphate-G (CpG) island (3478 base pairs) methylation in salivary gland adenoid cystic carcinoma. Phosphates 87-96 RUNX family transcription factor 3 Homo sapiens 78-83 22025728-4 2011 This finding correlated with enhanced repressive histone marks at the Cd8a promoter in the absence of E8(I), and the down-regulation of CD8alpha expression could be blocked by treating E8(I)-, Runx3-, or CBFbeta-deficient CD8(+) T cells with the histone deacetylase inhibitor trichostatin A. trichostatin A 276-290 RUNX family transcription factor 3 Homo sapiens 193-198 22246363-3 2011 SYBR Green I chimeric fluorescence Real-time PCR was applied to detect the expression of RUNX3 mRNA in 10 cases of normal cervix, 24 CIN, and 30 cervical carcinomas. sybr green 0-10 RUNX family transcription factor 3 Homo sapiens 89-94 21835883-3 2011 Our reporter assays and gene reactivation by 5-aza-2"-deoxycytidine, a DNA demethylating agent, show that DNA methylation occurring at CpG poor LAMB3 promoter and RUNX3 promoter 1(RUNX3 P1) can directly lead to transcriptional silencing in cells competent to express these genes in vitro. Decitabine 45-67 RUNX family transcription factor 3 Homo sapiens 163-168 21835883-3 2011 Our reporter assays and gene reactivation by 5-aza-2"-deoxycytidine, a DNA demethylating agent, show that DNA methylation occurring at CpG poor LAMB3 promoter and RUNX3 promoter 1(RUNX3 P1) can directly lead to transcriptional silencing in cells competent to express these genes in vitro. Decitabine 45-67 RUNX family transcription factor 3 Homo sapiens 180-185 22234069-8 2011 CONCLUSIONS: The serum RUNX3 promoter hypermethylation may be a promising biomarker for the early diagnosis of ESCC, GC and CRC, which was further confirmed by combining with CEA and CA19-9. ca19-9 183-189 RUNX family transcription factor 3 Homo sapiens 23-28 21567090-5 2011 Partial methylation was found in all 3 ACC cell lines, and the reactivation and more potent expression of RUNX3 was induced by 5-triazole-2-deoxycytidine. 5-triazole-2-deoxycytidine 127-153 RUNX family transcription factor 3 Homo sapiens 106-111 21612813-8 2011 RUNX3 knockdown resulted in a decrease in cell proliferation in liquid media as well as in soft agar. Agar 96-100 RUNX family transcription factor 3 Homo sapiens 0-5 22699781-9 2011 These results suggest that RUNX3 promoter methylation is a significant prognostic factor for overall survival in MIBC patients. 4-METHYL-2-PENTANOL 113-117 RUNX family transcription factor 3 Homo sapiens 27-32 21205092-5 2011 Moreover, the decreased RUNX3 expression was related to a lower accumulation of acetylated histone H3 associated with RUNX3. acetylated histone 80-98 RUNX family transcription factor 3 Homo sapiens 24-29 21205092-5 2011 Moreover, the decreased RUNX3 expression was related to a lower accumulation of acetylated histone H3 associated with RUNX3. acetylated histone 80-98 RUNX family transcription factor 3 Homo sapiens 118-123 21205092-6 2011 In in vitro experiments, vorinostat, a member of a new class of highly potent histone deacetylase inhibitors, restored RUNX3 expression in Mz-ChA-2 cells. Vorinostat 25-35 RUNX family transcription factor 3 Homo sapiens 119-124 21205092-7 2011 Furthermore, vorinostat-induced RUNX3 significantly enhanced p21 expression and growth inhibition of Mz-ChA-2 cells through restoration of TGF-beta signaling. Vorinostat 13-23 RUNX family transcription factor 3 Homo sapiens 32-37 21205092-9 2011 Furthermore, vorinostat might hold promise for treating biliary tract cancer through enhancement of TGF-beta signaling by restoration of RUNX3. Vorinostat 13-23 RUNX family transcription factor 3 Homo sapiens 137-142 21068132-8 2011 The CIMP marker RUNX3 was the earliest CpG island showing significant change, followed by the CIMP markers NEUROG1 and CACNA1G at the hyperplastic polyp stage. Cyclic IMP 4-8 RUNX family transcription factor 3 Homo sapiens 16-21 24250365-4 2011 The effect of Runx3 transfection on cell proliferation was determined by MTT assay and the results were confirmed by the trypan blue dye exclusion method. monooxyethylene trimethylolpropane tristearate 73-76 RUNX family transcription factor 3 Homo sapiens 14-19 21558800-6 2011 Compared to AML3 cells, AML2 cells are more sensitive to the treatment of the DNA-damaging compounds (doxorubicin and etoposide) and a specific p53-inducing compound (nutlin-3). Doxorubicin 102-113 RUNX family transcription factor 3 Homo sapiens 24-28 21558800-6 2011 Compared to AML3 cells, AML2 cells are more sensitive to the treatment of the DNA-damaging compounds (doxorubicin and etoposide) and a specific p53-inducing compound (nutlin-3). Etoposide 118-127 RUNX family transcription factor 3 Homo sapiens 24-28 21511279-0 2011 Nicotinamide inhibits growth of carcinogen induced mouse bladder tumor and human bladder tumor xenograft through up-regulation of RUNX3 and p300. Niacinamide 0-12 RUNX family transcription factor 3 Homo sapiens 130-135 21511279-9 2011 The effect of nicotinamide on Runx3 methylation status and tumor growth was measured. Niacinamide 14-26 RUNX family transcription factor 3 Homo sapiens 30-35 21511279-12 2011 CONCLUSIONS: Results suggest that nicotinamide has preventive and therapeutic effects on tumorigenesis through multiple mechanisms of RUNX3 expression up-regulation. Niacinamide 34-46 RUNX family transcription factor 3 Homo sapiens 134-139 21781566-2 2011 METHODS: Methylation-specific PCR and immunohistochemical SP technique were used to detect the methylation of RUNX3 gene promoter and expression of its protein in 56 cases of PTC and their matched adjacent non-carcinous epithelium (NCE). TFF2 protein, human 58-60 RUNX family transcription factor 3 Homo sapiens 110-115 20353948-0 2010 RUNX3 modulates DNA damage-mediated phosphorylation of tumor suppressor p53 at Ser-15 and acts as a co-activator for p53. Serine 79-82 RUNX family transcription factor 3 Homo sapiens 0-5 21223819-2 2010 METHODS: RT-PCR (reverse transcription-polymerase chain reaction), laser scanning confocal microscope (LSCM) and Western blot were used to detect the expression of RUNX3 gene and protein in salivary gland adenoid cystic carcinoma cell lines, ACC-2, ACC-3, and ACC-M, before/after a treatment of 5-Aza-dc respectively. Decitabine 295-303 RUNX family transcription factor 3 Homo sapiens 164-169 21223819-5 2010 After a treatment of 300 nmol/L 5-Aza-dc for 72 hours, the expression of RUNX3 in ACC-2 and ACC-3 cells was enhanced, and in ACC-M was restored. Decitabine 32-40 RUNX family transcription factor 3 Homo sapiens 73-78 21223819-7 2010 After a treatment of 300 nmol/L 5-Aza-dc for 72 h, both nuclear and cytoplasmic location of RUNX3 positive signals were found in the ACC-2 and ACC-3 cells. Decitabine 32-40 RUNX family transcription factor 3 Homo sapiens 92-97 21223819-11 2010 After a treatment of 5-Aza-dc, the RUNX3 gene showed unmethylated status in all three cell lines. Decitabine 21-29 RUNX family transcription factor 3 Homo sapiens 35-40 20353948-2 2010 In this study, we found that RUNX3 is closely involved in DNA damage-dependent phosphorylation of tumor suppressor p53 at Ser-15 and acts as a co-activator for p53. Serine 122-125 RUNX family transcription factor 3 Homo sapiens 29-34 20353948-3 2010 The small interference RNA-mediated knockdown of RUNX3 inhibited adriamycin (ADR)-dependent apoptosis in p53-proficient cells but not in p53-deficient cells in association with a significant reduction of p53-target gene expression as well as phosphorylation of p53 at Ser-15. Doxorubicin 65-75 RUNX family transcription factor 3 Homo sapiens 49-54 20353948-3 2010 The small interference RNA-mediated knockdown of RUNX3 inhibited adriamycin (ADR)-dependent apoptosis in p53-proficient cells but not in p53-deficient cells in association with a significant reduction of p53-target gene expression as well as phosphorylation of p53 at Ser-15. Serine 268-271 RUNX family transcription factor 3 Homo sapiens 49-54 20353948-8 2010 Additionally, RUNX3 had an ability to induce the phosphorylation of p53 at Ser-15, thereby promoting p53-dependent apoptosis. Serine 75-78 RUNX family transcription factor 3 Homo sapiens 14-19 20353948-11 2010 Thus, our present results strongly suggest that RUNX3 acts as a novel co-activator for p53 through regulating its DNA damage-induced phosphorylation at Ser-15 and also provide a clue to understanding the molecular mechanisms underlying RUNX3-mediated tumor suppression. Serine 152-155 RUNX family transcription factor 3 Homo sapiens 48-53 18848767-0 2009 5-Aza-2"-deoxycytidine reactivates expression of RUNX3 by deletion of DNA methyltransferases leading to caspase independent apoptosis in colorectal cancer Lovo cells. Decitabine 0-22 RUNX family transcription factor 3 Homo sapiens 49-54 20100835-0 2010 Src kinase phosphorylates RUNX3 at tyrosine residues and localizes the protein in the cytoplasm. Tyrosine 35-43 RUNX family transcription factor 3 Homo sapiens 26-31 20100835-6 2010 We also found that the tyrosine residues of endogenous RUNX3 are phosphorylated and that the protein is localized in the cytoplasm in Src-activated cancer cell lines. Tyrosine 23-31 RUNX family transcription factor 3 Homo sapiens 55-60 20100835-8 2010 Collectively, our results demonstrate that the tyrosine phosphorylation of RUNX3 by activated Src is associated with the cytoplasmic localization of RUNX3 in gastric and breast cancers. Tyrosine 47-55 RUNX family transcription factor 3 Homo sapiens 75-80 20100835-8 2010 Collectively, our results demonstrate that the tyrosine phosphorylation of RUNX3 by activated Src is associated with the cytoplasmic localization of RUNX3 in gastric and breast cancers. Tyrosine 47-55 RUNX family transcription factor 3 Homo sapiens 149-154 19764999-8 2009 Folate levels in tumors correlated positively with LINE-1, CDH13, and RUNX3 methylation. Folic Acid 0-6 RUNX family transcription factor 3 Homo sapiens 70-75 19763613-5 2009 The methylation level of examined genes was significantly higher in BilIN than in normal samples (TMEFF2, HOXA1, NEUROG1, and RUNX3, P < 0.05) and in EHC than in BilIN samples (TMEFF2, HOXA1, NEUROG1, RUNX3, RASSF1A, and APC, P < 0.05). Bile Pigments 68-73 RUNX family transcription factor 3 Homo sapiens 126-131 19763613-5 2009 The methylation level of examined genes was significantly higher in BilIN than in normal samples (TMEFF2, HOXA1, NEUROG1, and RUNX3, P < 0.05) and in EHC than in BilIN samples (TMEFF2, HOXA1, NEUROG1, RUNX3, RASSF1A, and APC, P < 0.05). Bile Pigments 68-73 RUNX family transcription factor 3 Homo sapiens 204-209 20350534-3 2010 Three doxorubicin-resistant AML cell lines (AML-2/DX30, AML-2/DX100, AML-2/DX300) were prepared via long-term exposure to doxorubicin for more than 3 months. Doxorubicin 6-17 RUNX family transcription factor 3 Homo sapiens 44-49 20350534-7 2010 Furthermore, resveratrol treatment induced a significant increase in the uptake of 5(6)-carboxyfluorescein diacetate, a MRP1 substrate, into the doxorubicin-resistant AML-2/DX300 cells. Resveratrol 13-24 RUNX family transcription factor 3 Homo sapiens 167-172 20350534-7 2010 Furthermore, resveratrol treatment induced a significant increase in the uptake of 5(6)-carboxyfluorescein diacetate, a MRP1 substrate, into the doxorubicin-resistant AML-2/DX300 cells. 5(6)-Carboxyfluorescein diacetate 83-116 RUNX family transcription factor 3 Homo sapiens 167-172 20350534-7 2010 Furthermore, resveratrol treatment induced a significant increase in the uptake of 5(6)-carboxyfluorescein diacetate, a MRP1 substrate, into the doxorubicin-resistant AML-2/DX300 cells. Doxorubicin 145-156 RUNX family transcription factor 3 Homo sapiens 167-172 20236534-8 2010 We show that the teleost Runx2 orthologue as well as the three mammalian Runx1, Runx2 and Runx3 paralogues are able to co-immunoprecipitate with the VDR protein present in nuclear extracts of rat osteoblasts stimulated with 1alpha,25-dihydroxyvitamin D3. 25-dihydroxyvitamin d3 231-253 RUNX family transcription factor 3 Homo sapiens 90-95 20236534-13 2010 Therefore, 1alpha,25-dihydroxyvitamin D3 might have been able to modulate the transcriptional activity of Runx1, Runx2 or Runx3 in the tissues expressing VDR. Calcitriol 11-40 RUNX family transcription factor 3 Homo sapiens 122-127 19695681-4 2009 In this study, we determined the methylation frequency of 5 genes, including p16, Runx3, MGMT, DAPK, and RASSF1A, by methylation-specific polymerase chain reaction, in a series of formalin-fixed paraffin-embedded tissues including normal gastric mucosa (n = 20), intestinal metaplasia (n = 14), gastric epithelial dysplasia (n = 27), and early gastric adenocarcinoma (n = 16). Formaldehyde 180-188 RUNX family transcription factor 3 Homo sapiens 82-87 19808967-5 2009 MDM2 blocks RUNX3 transcriptional activity by interacting with RUNX3 through an acidic domain adjacent to the p53-binding domain of MDM2 and ubiquitinates RUNX3 on key lysine residues to mediate nuclear export and proteasomal degradation. Lysine 168-174 RUNX family transcription factor 3 Homo sapiens 12-17 19808967-5 2009 MDM2 blocks RUNX3 transcriptional activity by interacting with RUNX3 through an acidic domain adjacent to the p53-binding domain of MDM2 and ubiquitinates RUNX3 on key lysine residues to mediate nuclear export and proteasomal degradation. Lysine 168-174 RUNX family transcription factor 3 Homo sapiens 63-68 19808967-5 2009 MDM2 blocks RUNX3 transcriptional activity by interacting with RUNX3 through an acidic domain adjacent to the p53-binding domain of MDM2 and ubiquitinates RUNX3 on key lysine residues to mediate nuclear export and proteasomal degradation. Lysine 168-174 RUNX family transcription factor 3 Homo sapiens 63-68 18850007-5 2009 This downregulation was abolished following treatment with the histone deacetylase (HDAC) inhibitor trichostatin A (TSA) and cytosine methylation inhibitor 5-aza-2-deoxycytidine (5-Aza), suggesting that an epigenetic regulatory mechanism may be involved in RUNX3 silencing by hypoxia. trichostatin A 100-114 RUNX family transcription factor 3 Homo sapiens 257-262 19645591-7 2009 RUNX3 methylation was further assessed by MSP and RT-PCR before and after 5-aza-2"-deoxycytidine (5-aza-dc) treatment in normal and cancer cell lines. Decitabine 74-96 RUNX family transcription factor 3 Homo sapiens 0-5 19645591-7 2009 RUNX3 methylation was further assessed by MSP and RT-PCR before and after 5-aza-2"-deoxycytidine (5-aza-dc) treatment in normal and cancer cell lines. Decitabine 98-106 RUNX family transcription factor 3 Homo sapiens 0-5 19287976-2 2009 To elucidate mechanism responsible for the development of resistance to Ara-C, we established the Ara-C resistant AML-2/WT cell sublines, AML-2/IDAC and AML-2/ARC. Cytarabine 72-77 RUNX family transcription factor 3 Homo sapiens 114-119 19287976-2 2009 To elucidate mechanism responsible for the development of resistance to Ara-C, we established the Ara-C resistant AML-2/WT cell sublines, AML-2/IDAC and AML-2/ARC. Cytarabine 98-103 RUNX family transcription factor 3 Homo sapiens 114-119 19287976-2 2009 To elucidate mechanism responsible for the development of resistance to Ara-C, we established the Ara-C resistant AML-2/WT cell sublines, AML-2/IDAC and AML-2/ARC. Cytarabine 98-103 RUNX family transcription factor 3 Homo sapiens 138-143 19287976-2 2009 To elucidate mechanism responsible for the development of resistance to Ara-C, we established the Ara-C resistant AML-2/WT cell sublines, AML-2/IDAC and AML-2/ARC. Cytarabine 98-103 RUNX family transcription factor 3 Homo sapiens 138-143 19287976-4 2009 The results of the microarray analysis revealed a severe defect in the expression of deoxycytidine kinase (dCK), which plays a key role in the transformation of Ara-C to the active form in AML-2/IDAC cells. Cytarabine 161-166 RUNX family transcription factor 3 Homo sapiens 189-194 19159630-0 2009 Possible involvement of activation of P53/P21 and demethylation of RUNX 3 in the cytotoxicity against Lovo cells induced by 5-Aza-2"-deoxycytidine. Decitabine 124-146 RUNX family transcription factor 3 Homo sapiens 67-73 18850007-5 2009 This downregulation was abolished following treatment with the histone deacetylase (HDAC) inhibitor trichostatin A (TSA) and cytosine methylation inhibitor 5-aza-2-deoxycytidine (5-Aza), suggesting that an epigenetic regulatory mechanism may be involved in RUNX3 silencing by hypoxia. trichostatin A 116-119 RUNX family transcription factor 3 Homo sapiens 257-262 18850007-5 2009 This downregulation was abolished following treatment with the histone deacetylase (HDAC) inhibitor trichostatin A (TSA) and cytosine methylation inhibitor 5-aza-2-deoxycytidine (5-Aza), suggesting that an epigenetic regulatory mechanism may be involved in RUNX3 silencing by hypoxia. Decitabine 156-177 RUNX family transcription factor 3 Homo sapiens 257-262 18850007-5 2009 This downregulation was abolished following treatment with the histone deacetylase (HDAC) inhibitor trichostatin A (TSA) and cytosine methylation inhibitor 5-aza-2-deoxycytidine (5-Aza), suggesting that an epigenetic regulatory mechanism may be involved in RUNX3 silencing by hypoxia. Decitabine 179-184 RUNX family transcription factor 3 Homo sapiens 257-262 18834226-3 2008 OBJECTIVE: To investigate and compare the molecular and clinicopathologic features of CIMP-positive colorectal cancers defined by classic (p16, hMLH1, MINT1, MINT2, MINT31) and new (CACNA1G, IGF2, NEUROG1, RUNX3, SOCS1) CIMP panels. Cyclic IMP 86-90 RUNX family transcription factor 3 Homo sapiens 206-211 19087683-1 2008 OBJECTIVE: To investigate the effect of DNA methyltransferases inhibitor 5-aza-2"-deoxycytidine (5-Aza-CdR) on the histone H3-lysine 9 methylation status and gene expression of RUNX3 in human bladder tumor cells. Decitabine 73-95 RUNX family transcription factor 3 Homo sapiens 177-182 18602973-0 2008 2,3,7,8-Tetrachlorodibenzo-p-dioxin modulates the expression of cKrox and Runx3, transcription regulatory factors controlling the lineage commitment of CD4+CD8+ into CD4 and CD8 thymocytes, respectively. Polychlorinated Dibenzodioxins 0-35 RUNX family transcription factor 3 Homo sapiens 74-79 18602973-3 2008 In the present study, we first demonstrated that the expression of transcription regulatory factors such as cKrox and Runx3, which have been shown to be intimately associated with the commitment of CD4+CD8+ double-positive (DP) to CD4 or CD8 single-positive (SP) thymocyes, was down-regulated by TCDD in CD4 SP thymocytes, but up-regulated in DP, CD4+CD8+ double-negative (DN), and CD8 SP thymocytes. sp 259-261 RUNX family transcription factor 3 Homo sapiens 118-123 18602973-3 2008 In the present study, we first demonstrated that the expression of transcription regulatory factors such as cKrox and Runx3, which have been shown to be intimately associated with the commitment of CD4+CD8+ double-positive (DP) to CD4 or CD8 single-positive (SP) thymocyes, was down-regulated by TCDD in CD4 SP thymocytes, but up-regulated in DP, CD4+CD8+ double-negative (DN), and CD8 SP thymocytes. Polychlorinated Dibenzodioxins 296-300 RUNX family transcription factor 3 Homo sapiens 118-123 18602973-4 2008 Then, we found that TCDD inhibited the differentiation of DPK cells, an immature CD4+CD8+ lymphoma cell line, into CD4+CD8(-) T cells, as well as the expression of cKrox and Runx3 upon antigen stimulation. Polychlorinated Dibenzodioxins 20-24 RUNX family transcription factor 3 Homo sapiens 174-179 19087683-3 2008 Other EJ cells were cultured and treated with 5-Aza-CdR and then chromatin immunoprecipitation assay was used to analyze the histone H3-lysine 9 methylation status of RUNX3 promoter and the second exon. histone h3-lysine 125-142 RUNX family transcription factor 3 Homo sapiens 167-172 19087683-11 2008 H3-lysine 9 trimethylation may be one of the most important reasons for gene inactivation of the RUNX3 gene. h3-lysine 0-9 RUNX family transcription factor 3 Homo sapiens 97-102 18360721-2 2008 In this study, we developed an AML cell line (AML-2/IDAC) that is resistant to treatment with a combination of idarubicin and cytosine arabinoside (Id/AraC) by chronic exposure for more than 3 months. Idarubicin 111-121 RUNX family transcription factor 3 Homo sapiens 46-51 18628431-6 2008 Tumors were classified as CIMP positive when at least three of five markers (RUNX3, CACNA1G, SOCS1, NEUROG1, and IGF2) were methylated according to MethyLight analysis. Cyclic IMP 26-30 RUNX family transcription factor 3 Homo sapiens 77-82 18430739-6 2008 RUNX3 was repressed by histone deacetylation and hypermethylation of a CpG island in the promoter region and restored by trichostatin A or/and 5-aza-2"-deoxycytidine. trichostatin A 121-135 RUNX family transcription factor 3 Homo sapiens 0-5 18430739-6 2008 RUNX3 was repressed by histone deacetylation and hypermethylation of a CpG island in the promoter region and restored by trichostatin A or/and 5-aza-2"-deoxycytidine. Decitabine 143-165 RUNX family transcription factor 3 Homo sapiens 0-5 18494051-6 2008 The activated level of RUNX3 was examined after treatment with the different density of 5"-aza-2"-deoxycytidine (5-Aza-CdR) by using semi-quantitative RT-PCR and Western blotting. Decitabine 88-111 RUNX family transcription factor 3 Homo sapiens 23-28 18360721-2 2008 In this study, we developed an AML cell line (AML-2/IDAC) that is resistant to treatment with a combination of idarubicin and cytosine arabinoside (Id/AraC) by chronic exposure for more than 3 months. Cytarabine 126-146 RUNX family transcription factor 3 Homo sapiens 46-51 18360721-3 2008 We then investigated the ability of indomethacin to alleviate the chemoresistance of AML-2/IDAC cells. Indomethacin 36-48 RUNX family transcription factor 3 Homo sapiens 85-90 18360721-5 2008 However, when AML-2/IDAC cells were treated with combinations of indomethacin and Id/AraC, the cell death and apoptosis rate of AML-2/IDAC cells were significantly increased in a dose- and time-dependent manner. Indomethacin 65-77 RUNX family transcription factor 3 Homo sapiens 14-19 18360721-5 2008 However, when AML-2/IDAC cells were treated with combinations of indomethacin and Id/AraC, the cell death and apoptosis rate of AML-2/IDAC cells were significantly increased in a dose- and time-dependent manner. Indomethacin 65-77 RUNX family transcription factor 3 Homo sapiens 128-133 18360721-6 2008 The combined treatment with indomethacin and Id/AraC caused the collapse of the mitochondrial membrane potential and was also demonstrated to enhance the activities of caspase-3 and -8 in AML-2/IDAC cells. Indomethacin 28-40 RUNX family transcription factor 3 Homo sapiens 188-193 18360721-6 2008 The combined treatment with indomethacin and Id/AraC caused the collapse of the mitochondrial membrane potential and was also demonstrated to enhance the activities of caspase-3 and -8 in AML-2/IDAC cells. Cytarabine 48-52 RUNX family transcription factor 3 Homo sapiens 188-193 18360721-7 2008 Furthermore, indomethacin down-regulated expression of the ABCA3 and MRP1 genes, which were over-expressed in AML-2/IDAC cells. Indomethacin 13-25 RUNX family transcription factor 3 Homo sapiens 110-115 17956589-3 2008 In the present study, we constructed an adenoviral vector encoding human RUNX3 cDNA under the control of a Tet-responsive promoter (Ad-Tet-FLAG-RUNX3), which regulates the expression of RUNX3 in the presence or absence of doxycycline. tetramethylenedisulfotetramine 107-110 RUNX family transcription factor 3 Homo sapiens 73-78 18426645-6 2008 It is concluded that methylation of runx3 gene promoter probably plays a role in the pathogenesis of AL and may have clinical significance in predicting prognosis of AL. Aluminum 101-103 RUNX family transcription factor 3 Homo sapiens 36-41 18426645-6 2008 It is concluded that methylation of runx3 gene promoter probably plays a role in the pathogenesis of AL and may have clinical significance in predicting prognosis of AL. Aluminum 166-168 RUNX family transcription factor 3 Homo sapiens 36-41 17956589-3 2008 In the present study, we constructed an adenoviral vector encoding human RUNX3 cDNA under the control of a Tet-responsive promoter (Ad-Tet-FLAG-RUNX3), which regulates the expression of RUNX3 in the presence or absence of doxycycline. tetramethylenedisulfotetramine 107-110 RUNX family transcription factor 3 Homo sapiens 144-149 17956589-3 2008 In the present study, we constructed an adenoviral vector encoding human RUNX3 cDNA under the control of a Tet-responsive promoter (Ad-Tet-FLAG-RUNX3), which regulates the expression of RUNX3 in the presence or absence of doxycycline. tetramethylenedisulfotetramine 107-110 RUNX family transcription factor 3 Homo sapiens 144-149 17956589-3 2008 In the present study, we constructed an adenoviral vector encoding human RUNX3 cDNA under the control of a Tet-responsive promoter (Ad-Tet-FLAG-RUNX3), which regulates the expression of RUNX3 in the presence or absence of doxycycline. tetramethylenedisulfotetramine 135-138 RUNX family transcription factor 3 Homo sapiens 73-78 17956589-3 2008 In the present study, we constructed an adenoviral vector encoding human RUNX3 cDNA under the control of a Tet-responsive promoter (Ad-Tet-FLAG-RUNX3), which regulates the expression of RUNX3 in the presence or absence of doxycycline. tetramethylenedisulfotetramine 135-138 RUNX family transcription factor 3 Homo sapiens 144-149 17956589-3 2008 In the present study, we constructed an adenoviral vector encoding human RUNX3 cDNA under the control of a Tet-responsive promoter (Ad-Tet-FLAG-RUNX3), which regulates the expression of RUNX3 in the presence or absence of doxycycline. tetramethylenedisulfotetramine 135-138 RUNX family transcription factor 3 Homo sapiens 144-149 17956589-3 2008 In the present study, we constructed an adenoviral vector encoding human RUNX3 cDNA under the control of a Tet-responsive promoter (Ad-Tet-FLAG-RUNX3), which regulates the expression of RUNX3 in the presence or absence of doxycycline. Doxycycline 222-233 RUNX family transcription factor 3 Homo sapiens 73-78 17956589-3 2008 In the present study, we constructed an adenoviral vector encoding human RUNX3 cDNA under the control of a Tet-responsive promoter (Ad-Tet-FLAG-RUNX3), which regulates the expression of RUNX3 in the presence or absence of doxycycline. Doxycycline 222-233 RUNX family transcription factor 3 Homo sapiens 144-149 17956589-3 2008 In the present study, we constructed an adenoviral vector encoding human RUNX3 cDNA under the control of a Tet-responsive promoter (Ad-Tet-FLAG-RUNX3), which regulates the expression of RUNX3 in the presence or absence of doxycycline. Doxycycline 222-233 RUNX family transcription factor 3 Homo sapiens 144-149 17956589-5 2008 The effect of the transduction of RUNX3 on cell growth was examined using the Tet-On system in a human gastric carcinoma cell line, MKN-1. tetramethylenedisulfotetramine 78-81 RUNX family transcription factor 3 Homo sapiens 34-39 17956589-6 2008 Exogenous RUNX3 expression was induced successfully by Ad-Tet-FLAG-RUNX3, but not Ad-Tet-LacZ, in the presence of doxycycline in the MKN-1 cells. Doxycycline 114-125 RUNX family transcription factor 3 Homo sapiens 10-15 17956589-8 2008 Flow cytometry revealed that the sub-G(1) peak was increased in cells expressing RUNX3 (34.11%), indicating that the inhibition of cell growth was due to apoptosis, which was confirmed based on Hoechst 33258 staining, the release of cytochrome c from mitochondria into the cytosol, and detection of cleaved caspase-3 by western blotting in MKN-1 cells. hoechst 194-201 RUNX family transcription factor 3 Homo sapiens 81-86 17898258-8 2007 The rates for the CIMP-related genes were 25% for RUNX3, 5% for NEUROG1 and CACNA1G, and 0 for SOCS-1 and IGF-2. Cyclic IMP 18-22 RUNX family transcription factor 3 Homo sapiens 50-55 17218010-0 2007 Balance of NF-kappaB and p38 MAPK is a determinant of radiosensitivity of the AML-2 and its doxorubicin-resistant cell lines. Doxorubicin 92-103 RUNX family transcription factor 3 Homo sapiens 78-83 17218010-3 2007 AML-2/DX100 characterized by down-regulated catalase expression was supersensitive to exogenous hydrogen peroxide whereas they increased defense mechanisms against endogenous reactive oxygen species (ROS) as compared with AML-2/WT. Hydrogen Peroxide 96-113 RUNX family transcription factor 3 Homo sapiens 0-5 17276407-0 2007 Contribution of reactivated RUNX3 to inhibition of gastric cancer cell growth following suberoylanilide hydroxamic acid (vorinostat) treatment. Vorinostat 88-119 RUNX family transcription factor 3 Homo sapiens 28-33 17218010-3 2007 AML-2/DX100 characterized by down-regulated catalase expression was supersensitive to exogenous hydrogen peroxide whereas they increased defense mechanisms against endogenous reactive oxygen species (ROS) as compared with AML-2/WT. Reactive Oxygen Species 175-198 RUNX family transcription factor 3 Homo sapiens 0-5 17218010-3 2007 AML-2/DX100 characterized by down-regulated catalase expression was supersensitive to exogenous hydrogen peroxide whereas they increased defense mechanisms against endogenous reactive oxygen species (ROS) as compared with AML-2/WT. Reactive Oxygen Species 200-203 RUNX family transcription factor 3 Homo sapiens 0-5 17218010-6 2007 A specific p38 MAPK inhibitor SB203580 increased radioresistance in AML-2/WT but little in AML-2/DX100. SB 203580 30-38 RUNX family transcription factor 3 Homo sapiens 68-73 17218010-10 2007 Taken together, these results indicate that radioresistance mechanisms of AML-2/DX100 could be related to alterations in ROS-scavenging activity, in mitochondrial translocation of Bax and Bcl-2, and in expression of pro-apoptotic (granzyme H) and anti-apoptotic (Bfl-1/A1) genes. Reactive Oxygen Species 121-124 RUNX family transcription factor 3 Homo sapiens 74-79 17384682-7 2007 Stable transfection of esophageal cancer cells with RUNX3 slightly inhibited cell proliferation in vitro, enhanced the antiproliferative and apoptotic effects of TGF-beta and increased radiosensitivity in conjunction with Bim induction. bim 222-225 RUNX family transcription factor 3 Homo sapiens 52-57 17384682-9 2007 Treatment with 5-aza-2"-deoxycytidine restored RUNX3 expression, increased radiosensitivity and induced Bim in both control and radioresistant cells. Decitabine 15-37 RUNX family transcription factor 3 Homo sapiens 47-52 21783769-2 2007 The purpose of this study was to investigate the Pgp-reversal activities of phthalates, which are endocrine-disrupting chemicals, by utilizing the Pgp-overexpressing leukemic cell line AML-2/D100. phthalic acid 76-86 RUNX family transcription factor 3 Homo sapiens 185-190 17276407-0 2007 Contribution of reactivated RUNX3 to inhibition of gastric cancer cell growth following suberoylanilide hydroxamic acid (vorinostat) treatment. Vorinostat 121-131 RUNX family transcription factor 3 Homo sapiens 28-33 17276407-3 2007 This study investigates the role of RUNX3 in vorinostat-induced suppression of gastric cancer cell growth. Vorinostat 45-55 RUNX family transcription factor 3 Homo sapiens 36-41 16997801-3 2006 This study was designed to investigate the role of reactive oxygen species (ROS) and glutathione on the resistance of AML-2/DX100 cells to mercuric chloride. Reactive Oxygen Species 51-74 RUNX family transcription factor 3 Homo sapiens 118-123 17276407-4 2007 RUNX3 was up-regulated by vorinostat in gastric cancer cell lines not expressing RUNX3. Vorinostat 26-36 RUNX family transcription factor 3 Homo sapiens 0-5 17276407-5 2007 In terms of cell viability, the mean IC(50) of vorinostat in RUNX3-negative cells was significantly lower than that seen in RUNX3-positive cells, indicating that the former are more sensitive to vorinostat in terms of growth arrest than are RUNX3-positive lines. Vorinostat 47-57 RUNX family transcription factor 3 Homo sapiens 61-66 17276407-6 2007 The mechanism underlying this difference was found to be reactivation of RUNX3 expression by vorinostat and concomitant increase in acetylated histone H3 in the promoter region of RUNX3. Vorinostat 93-103 RUNX family transcription factor 3 Homo sapiens 73-78 17276407-7 2007 Using three RUNX3-negative cell lines, we determined the contribution of RUNX3 reactivation to growth inhibition and induction of apoptosis following treatment of cells with vorinostat and found that up-regulated RUNX3 was significantly responsible for tumor suppressive activities. Vorinostat 174-184 RUNX family transcription factor 3 Homo sapiens 12-17 17276407-7 2007 Using three RUNX3-negative cell lines, we determined the contribution of RUNX3 reactivation to growth inhibition and induction of apoptosis following treatment of cells with vorinostat and found that up-regulated RUNX3 was significantly responsible for tumor suppressive activities. Vorinostat 174-184 RUNX family transcription factor 3 Homo sapiens 73-78 17276407-7 2007 Using three RUNX3-negative cell lines, we determined the contribution of RUNX3 reactivation to growth inhibition and induction of apoptosis following treatment of cells with vorinostat and found that up-regulated RUNX3 was significantly responsible for tumor suppressive activities. Vorinostat 174-184 RUNX family transcription factor 3 Homo sapiens 73-78 16997801-0 2006 Elevated reactive oxygen species but not glutathione regulate mercury resistance to AML-2/DX100 cells. Reactive Oxygen Species 9-32 RUNX family transcription factor 3 Homo sapiens 84-89 17270239-6 2007 After stratification by sex, location, tumor differentiation, RUNX3 status, KRAS/BRAF status, or p53 status, CIMP-high was persistently correlated with TGFBR2 mutation. Cyclic IMP 109-113 RUNX family transcription factor 3 Homo sapiens 62-67 17360569-9 2007 Proviral integration near the RUNX3 promoter induced RUNX3 expression, and Bcr-Abl-positive cell lines with stable or inducible expression of RUNX1 or RUNX3 were protected from imatinib-induced apoptosis. Imatinib Mesylate 177-185 RUNX family transcription factor 3 Homo sapiens 30-35 17360569-9 2007 Proviral integration near the RUNX3 promoter induced RUNX3 expression, and Bcr-Abl-positive cell lines with stable or inducible expression of RUNX1 or RUNX3 were protected from imatinib-induced apoptosis. Imatinib Mesylate 177-185 RUNX family transcription factor 3 Homo sapiens 53-58 17360569-9 2007 Proviral integration near the RUNX3 promoter induced RUNX3 expression, and Bcr-Abl-positive cell lines with stable or inducible expression of RUNX1 or RUNX3 were protected from imatinib-induced apoptosis. Imatinib Mesylate 177-185 RUNX family transcription factor 3 Homo sapiens 53-58 16458935-2 2006 In order to investigate the genes involved in drug resistance, a human leukemia cell line that is resistant to doxorubicin, an anthracycline anticancer agent (AML-2/DX100), was selected and its gene expression profile was analyzed using a cDNA microarray. Doxorubicin 111-122 RUNX family transcription factor 3 Homo sapiens 159-164 16458935-2 2006 In order to investigate the genes involved in drug resistance, a human leukemia cell line that is resistant to doxorubicin, an anthracycline anticancer agent (AML-2/DX100), was selected and its gene expression profile was analyzed using a cDNA microarray. Anthracyclines 127-140 RUNX family transcription factor 3 Homo sapiens 159-164 16458935-5 2006 The AML-2/DX100 cells were also resistant to other anticancer drugs, including daunorubicin and camptothecin, and the expression levels of the differentially regulated genes such as STMN1, MMP-2 and CTSG, were constantly maintained. Daunorubicin 79-91 RUNX family transcription factor 3 Homo sapiens 4-9 16458935-5 2006 The AML-2/DX100 cells were also resistant to other anticancer drugs, including daunorubicin and camptothecin, and the expression levels of the differentially regulated genes such as STMN1, MMP-2 and CTSG, were constantly maintained. Camptothecin 96-108 RUNX family transcription factor 3 Homo sapiens 4-9 16997801-0 2006 Elevated reactive oxygen species but not glutathione regulate mercury resistance to AML-2/DX100 cells. Mercury 62-69 RUNX family transcription factor 3 Homo sapiens 84-89 16997801-3 2006 This study was designed to investigate the role of reactive oxygen species (ROS) and glutathione on the resistance of AML-2/DX100 cells to mercuric chloride. Reactive Oxygen Species 76-79 RUNX family transcription factor 3 Homo sapiens 118-123 16997801-3 2006 This study was designed to investigate the role of reactive oxygen species (ROS) and glutathione on the resistance of AML-2/DX100 cells to mercuric chloride. Glutathione 85-96 RUNX family transcription factor 3 Homo sapiens 118-123 16997801-4 2006 The MRP1 overexpressing cells (AML-2/DX100) cells showed less scavenging activity to ROS induced by mercury while no difference in the basal glutathione levels between AML-2/WT and AML-2/DX100 cells. Reactive Oxygen Species 85-88 RUNX family transcription factor 3 Homo sapiens 31-36 16997801-4 2006 The MRP1 overexpressing cells (AML-2/DX100) cells showed less scavenging activity to ROS induced by mercury while no difference in the basal glutathione levels between AML-2/WT and AML-2/DX100 cells. Mercury 100-107 RUNX family transcription factor 3 Homo sapiens 31-36 16997801-5 2006 Mercury induced the activation of p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK) but not c-jun-N-terminal kinase in AML-2/DX100 cells. Mercury 0-7 RUNX family transcription factor 3 Homo sapiens 161-166 16997801-6 2006 The specific inhibitor for p38 MAPK and ERK, and antioxidant decreased the production of MRP1 and therefore resistance of AML-2/DX100 cells against mercury exposure. Mercury 148-155 RUNX family transcription factor 3 Homo sapiens 122-127 16997801-7 2006 These results suggest that induction of ROS and downstream p38 MAPK and ERK were involved in the resistance of cells to mercury by expression MRP1 in AML-2/DX100 cells. Reactive Oxygen Species 40-43 RUNX family transcription factor 3 Homo sapiens 150-155 16997801-7 2006 These results suggest that induction of ROS and downstream p38 MAPK and ERK were involved in the resistance of cells to mercury by expression MRP1 in AML-2/DX100 cells. Mercury 120-127 RUNX family transcription factor 3 Homo sapiens 150-155 16328045-6 2006 RUNX3 expression was restored by treatment with 5-aza-2"-deoxycytidine and/or trichostatin-A in AdC cell lines. Decitabine 48-70 RUNX family transcription factor 3 Homo sapiens 0-5 16328045-6 2006 RUNX3 expression was restored by treatment with 5-aza-2"-deoxycytidine and/or trichostatin-A in AdC cell lines. trichostatin A 78-92 RUNX family transcription factor 3 Homo sapiens 0-5 15386419-10 2005 Tricostatin A and 5"-azacitidin reactivate RUNX3 expression, but they could not reactivate expression of RUNX1 and CBFBeta in gastric cancer cells, suggesting that the downregulation was due to mechanisms other than methylation of the promoter region. trichostatin A 0-13 RUNX family transcription factor 3 Homo sapiens 43-48 15585369-6 2005 This study was designed to determine if mercury could be extruded by MRP1 in acute myeloid leukemia cells (AML-2). Mercury 40-47 RUNX family transcription factor 3 Homo sapiens 107-112 15585369-7 2005 The MRP-1-overexpressing AML-2/DX100 cells showed a higher resistance to mercury than AML-2/WT. Mercury 73-80 RUNX family transcription factor 3 Homo sapiens 25-30 15585369-9 2005 Exposing the AML-2 cells to mercury-induced MRP1 gene expression and production without altering the MRP1 activity. Mercury 28-35 RUNX family transcription factor 3 Homo sapiens 13-18 16155404-6 2005 Interestingly, demethylating agent 5-aza-2-deoxycytidine induced reactivation and more potent expression of RUNX3 gene in HCC cell lines. Decitabine 35-56 RUNX family transcription factor 3 Homo sapiens 108-113 15756676-7 2005 Flow cytometry examination suggested that expression of Runx3 in gastric cancer cells increased the intracellular accumulation and retention of adriamycin. Doxorubicin 144-154 RUNX family transcription factor 3 Homo sapiens 56-61 15685235-8 2005 The rate of downregulation of RUNX3 of adjacent mucosa was 39.2% (11 in 28 cases) in RB and 47.6% (10 in 21 cases) in RM, which are significantly higher than that of the GCI group (19.5%, 17 in 87 cases). Rubidium 85-87 RUNX family transcription factor 3 Homo sapiens 30-35 15685235-9 2005 In noncancerous mucosa of the remnant stomach in the RB group, RUNX3 expression decreased more near the anastomosis area. Rubidium 53-55 RUNX family transcription factor 3 Homo sapiens 63-68 15386419-10 2005 Tricostatin A and 5"-azacitidin reactivate RUNX3 expression, but they could not reactivate expression of RUNX1 and CBFBeta in gastric cancer cells, suggesting that the downregulation was due to mechanisms other than methylation of the promoter region. 5"-azacitidin 18-31 RUNX family transcription factor 3 Homo sapiens 43-48 15158439-2 2004 Their scavenging capacity against ROS was determined using a fluorometric probe in the doxorubicin-resistant AML-2/DX100 cell characterized by the down-regulation of catalase. Reactive Oxygen Species 34-37 RUNX family transcription factor 3 Homo sapiens 109-114 15386381-10 2004 RUNX3 promoter methylation was reversed and its expression restored in SW48 and HCT15 colon cancer cells after treatment with the demethylating agent 5-aza-2"-deoxycytidine, indicating that loss of expression is caused by epigenetic inactivation in colon carcinogenesis. Decitabine 150-172 RUNX family transcription factor 3 Homo sapiens 0-5 15273736-5 2004 The following observations were made: (i) RUNX3 was re-expressed after 5-aza-2"-deoxycytidine treatment, (ii) the RUNX3 promoter was found to be methylated by MS-PCR, and (iii) hypermethylation of the RUNX3 promoter was confirmed by direct sequencing analysis after sodium bisulfite modification in the above 12 cell lines. Decitabine 71-93 RUNX family transcription factor 3 Homo sapiens 42-47 15273736-5 2004 The following observations were made: (i) RUNX3 was re-expressed after 5-aza-2"-deoxycytidine treatment, (ii) the RUNX3 promoter was found to be methylated by MS-PCR, and (iii) hypermethylation of the RUNX3 promoter was confirmed by direct sequencing analysis after sodium bisulfite modification in the above 12 cell lines. Decitabine 71-93 RUNX family transcription factor 3 Homo sapiens 114-119 15273736-5 2004 The following observations were made: (i) RUNX3 was re-expressed after 5-aza-2"-deoxycytidine treatment, (ii) the RUNX3 promoter was found to be methylated by MS-PCR, and (iii) hypermethylation of the RUNX3 promoter was confirmed by direct sequencing analysis after sodium bisulfite modification in the above 12 cell lines. Decitabine 71-93 RUNX family transcription factor 3 Homo sapiens 114-119 15273736-5 2004 The following observations were made: (i) RUNX3 was re-expressed after 5-aza-2"-deoxycytidine treatment, (ii) the RUNX3 promoter was found to be methylated by MS-PCR, and (iii) hypermethylation of the RUNX3 promoter was confirmed by direct sequencing analysis after sodium bisulfite modification in the above 12 cell lines. sodium bisulfite 266-282 RUNX family transcription factor 3 Homo sapiens 42-47 15273736-5 2004 The following observations were made: (i) RUNX3 was re-expressed after 5-aza-2"-deoxycytidine treatment, (ii) the RUNX3 promoter was found to be methylated by MS-PCR, and (iii) hypermethylation of the RUNX3 promoter was confirmed by direct sequencing analysis after sodium bisulfite modification in the above 12 cell lines. sodium bisulfite 266-282 RUNX family transcription factor 3 Homo sapiens 114-119 15273736-5 2004 The following observations were made: (i) RUNX3 was re-expressed after 5-aza-2"-deoxycytidine treatment, (ii) the RUNX3 promoter was found to be methylated by MS-PCR, and (iii) hypermethylation of the RUNX3 promoter was confirmed by direct sequencing analysis after sodium bisulfite modification in the above 12 cell lines. sodium bisulfite 266-282 RUNX family transcription factor 3 Homo sapiens 114-119 15138260-4 2004 The p300-dependent acetylation of three lysine residues protects RUNX3 from ubiquitin ligase Smurf-mediated degradation. Lysine 40-46 RUNX family transcription factor 3 Homo sapiens 65-70 15138260-6 2004 Our findings demonstrate that the level of RUNX3 protein is controlled by the competitive acetylation and deacetylation of the three lysine residues, revealing a new mechanism for the posttranslational regulation of RUNX3 expression. Lysine 133-139 RUNX family transcription factor 3 Homo sapiens 43-48 15138260-6 2004 Our findings demonstrate that the level of RUNX3 protein is controlled by the competitive acetylation and deacetylation of the three lysine residues, revealing a new mechanism for the posttranslational regulation of RUNX3 expression. Lysine 133-139 RUNX family transcription factor 3 Homo sapiens 216-221 15158439-2 2004 Their scavenging capacity against ROS was determined using a fluorometric probe in the doxorubicin-resistant AML-2/DX100 cell characterized by the down-regulation of catalase. Doxorubicin 87-98 RUNX family transcription factor 3 Homo sapiens 109-114 15158439-3 2004 AML-2/DX100 cells had more scavenging capacity against endogenous pro-oxidants than did the parental cells AML-2/WT, suggesting that an anti-oxidant adaptation against ROS occurred. Reactive Oxygen Species 168-171 RUNX family transcription factor 3 Homo sapiens 0-5 12139723-0 2002 Superior effect of 9-cis retinoic acid (RA) compared with all-trans RA and 13-cis RA on the inhibition of clonogenic cell growth and the induction of apoptosis in OCI/AML-2 subclones: is the p53 pathway involved? Alitretinoin 19-38 RUNX family transcription factor 3 Homo sapiens 167-172 14743205-6 2004 Moreover, treatment with the methylation inhibitor 5"-aza-2"-deoxycitidine activated RUNX3 mRNA expression in all of 16 cancer cell lines that originally lacked RUNX3 expression. 5"-aza-2"-deoxycitidine 51-74 RUNX family transcription factor 3 Homo sapiens 85-90 14743205-6 2004 Moreover, treatment with the methylation inhibitor 5"-aza-2"-deoxycitidine activated RUNX3 mRNA expression in all of 16 cancer cell lines that originally lacked RUNX3 expression. 5"-aza-2"-deoxycitidine 51-74 RUNX family transcription factor 3 Homo sapiens 161-166 14500656-0 2003 Morpholino antisense oligonucleotide-mediated gene knockdown during thymocyte development reveals role for Runx3 transcription factor in CD4 silencing during development of CD4-/CD8+ thymocytes. Morpholinos 0-10 RUNX family transcription factor 3 Homo sapiens 107-112 14500656-0 2003 Morpholino antisense oligonucleotide-mediated gene knockdown during thymocyte development reveals role for Runx3 transcription factor in CD4 silencing during development of CD4-/CD8+ thymocytes. Oligonucleotides 21-36 RUNX family transcription factor 3 Homo sapiens 107-112 14500656-10 2003 The knockdown of Runx3 protein expression through morpholino oligonucleotides inhibited the development of CD4(-)/CD8(+) T cells. Morpholinos 50-77 RUNX family transcription factor 3 Homo sapiens 17-22 12139723-0 2002 Superior effect of 9-cis retinoic acid (RA) compared with all-trans RA and 13-cis RA on the inhibition of clonogenic cell growth and the induction of apoptosis in OCI/AML-2 subclones: is the p53 pathway involved? Tretinoin 40-42 RUNX family transcription factor 3 Homo sapiens 167-172 12139723-2 2002 The study was performed with the subclones of the retinoid-sensitive OCI/AML-2 cell line. Retinoids 50-58 RUNX family transcription factor 3 Homo sapiens 73-78 12139723-7 2002 In conclusion, this study shows that 9-cis RA was a more potent agent than ATRA or 13-cis RA in inducing growth arrest and apoptosis in the OCI/AML-2 subclones. Tretinoin 43-45 RUNX family transcription factor 3 Homo sapiens 144-149 11178967-0 2001 Down-regulation of catalase gene expression in the doxorubicin-resistant AML subline AML-2/DX100. Doxorubicin 51-62 RUNX family transcription factor 3 Homo sapiens 85-90 12127970-3 2002 Sinensetin reversed the resistance of P-glycoprotein (Pgp)-overexpressing AML-2/D100 to vincristine in a concentration-dependent manner. sinensetin 0-10 RUNX family transcription factor 3 Homo sapiens 74-79 12127970-3 2002 Sinensetin reversed the resistance of P-glycoprotein (Pgp)-overexpressing AML-2/D100 to vincristine in a concentration-dependent manner. Vincristine 88-99 RUNX family transcription factor 3 Homo sapiens 74-79 12127970-5 2002 Sinensetin cytotoxicity in AML-2/D100 was not changed by the complete inhibition of Pgp, suggesting that it is not a substrate for Pgp. sinensetin 0-10 RUNX family transcription factor 3 Homo sapiens 27-32 12127970-6 2002 Flow cytometry showed that sinensetin increased drug accumulation in the AML-2/D100 in a concentration-dependent manner. sinensetin 27-37 RUNX family transcription factor 3 Homo sapiens 73-78 11322768-3 2001 This study attempted not only to determine novel resistance mechanisms in MRP-overexpressing AML cells (AML-2/DX100) by chronic exposure to doxorubicin in the presence of an MRP inhibitor probenecid but also to find out whether probenecid could increase MRP levels. Doxorubicin 140-151 RUNX family transcription factor 3 Homo sapiens 104-109 11322768-3 2001 This study attempted not only to determine novel resistance mechanisms in MRP-overexpressing AML cells (AML-2/DX100) by chronic exposure to doxorubicin in the presence of an MRP inhibitor probenecid but also to find out whether probenecid could increase MRP levels. Probenecid 188-198 RUNX family transcription factor 3 Homo sapiens 104-109 11322768-4 2001 AML-2/DXPBA cultured in the presence of probenecid (600 microM) and doxorubicin (100 ng/ml) showed a higher level of the multidrug resistance (MDR) phenotype when compared to AML-2/DX100. Probenecid 40-50 RUNX family transcription factor 3 Homo sapiens 0-5 11322768-4 2001 AML-2/DXPBA cultured in the presence of probenecid (600 microM) and doxorubicin (100 ng/ml) showed a higher level of the multidrug resistance (MDR) phenotype when compared to AML-2/DX100. Probenecid 40-50 RUNX family transcription factor 3 Homo sapiens 175-180 11322768-4 2001 AML-2/DXPBA cultured in the presence of probenecid (600 microM) and doxorubicin (100 ng/ml) showed a higher level of the multidrug resistance (MDR) phenotype when compared to AML-2/DX100. Doxorubicin 68-79 RUNX family transcription factor 3 Homo sapiens 0-5 11322768-7 2001 Of the MRP inhibitors including probenecid, ofloxacin, erythromycin, and rifampicin used in this study, only probenecid showed a marked chemosensitizing effect in AML-2/DX100 but not in HL-60/Adr, suggesting that the chemosensitizing effects of the MRP inhibitors vary according to the type of resistant cells. Rifampin 73-83 RUNX family transcription factor 3 Homo sapiens 163-168 11322768-7 2001 Of the MRP inhibitors including probenecid, ofloxacin, erythromycin, and rifampicin used in this study, only probenecid showed a marked chemosensitizing effect in AML-2/DX100 but not in HL-60/Adr, suggesting that the chemosensitizing effects of the MRP inhibitors vary according to the type of resistant cells. Probenecid 109-119 RUNX family transcription factor 3 Homo sapiens 163-168 11178967-9 2001 Taken together, the paradoxical increase in the sensitivity of an MRP-overexpressing AML-2/DX100 in response to peroxides and paraquat is due to the down-regulation of catalase gene expression, which totally independent of overexpression of MRP. Peroxides 112-121 RUNX family transcription factor 3 Homo sapiens 85-90 11178967-2 2001 The previous study revealed that a doxorubicin-resistant AML subline (AML-2/DX100) overexpressed an MDR-associated protein (MRP) but not P-glycoprotein. Doxorubicin 35-46 RUNX family transcription factor 3 Homo sapiens 70-75 11178967-3 2001 The AML-2/DX100 also showed various levels of resistance to daunorubicin and vincristine but was paradoxically sensitive to hydrogen peroxide (5-fold), t-butyl hydroperoxide (3-fold), and paraquat (2-fold) when compared to the drug-sensitive parental AML-2 cells (AML-2/WT). Daunorubicin 60-72 RUNX family transcription factor 3 Homo sapiens 4-9 11178967-3 2001 The AML-2/DX100 also showed various levels of resistance to daunorubicin and vincristine but was paradoxically sensitive to hydrogen peroxide (5-fold), t-butyl hydroperoxide (3-fold), and paraquat (2-fold) when compared to the drug-sensitive parental AML-2 cells (AML-2/WT). Vincristine 77-88 RUNX family transcription factor 3 Homo sapiens 4-9 11178967-3 2001 The AML-2/DX100 also showed various levels of resistance to daunorubicin and vincristine but was paradoxically sensitive to hydrogen peroxide (5-fold), t-butyl hydroperoxide (3-fold), and paraquat (2-fold) when compared to the drug-sensitive parental AML-2 cells (AML-2/WT). Hydrogen Peroxide 124-141 RUNX family transcription factor 3 Homo sapiens 4-9 11178967-3 2001 The AML-2/DX100 also showed various levels of resistance to daunorubicin and vincristine but was paradoxically sensitive to hydrogen peroxide (5-fold), t-butyl hydroperoxide (3-fold), and paraquat (2-fold) when compared to the drug-sensitive parental AML-2 cells (AML-2/WT). tert-Butylhydroperoxide 152-173 RUNX family transcription factor 3 Homo sapiens 4-9 11178967-3 2001 The AML-2/DX100 also showed various levels of resistance to daunorubicin and vincristine but was paradoxically sensitive to hydrogen peroxide (5-fold), t-butyl hydroperoxide (3-fold), and paraquat (2-fold) when compared to the drug-sensitive parental AML-2 cells (AML-2/WT). Paraquat 188-196 RUNX family transcription factor 3 Homo sapiens 4-9 10774745-4 2000 They were also slightly more resistant than the parental cell (AML-2/WT) to etoposide, camptothecin and daunorubicin. Etoposide 76-85 RUNX family transcription factor 3 Homo sapiens 63-68 10774745-1 2000 Reactive oxygen species (ROS)-specific mechanisms of drug resistance were explored in paraquat (PQ)-resistant acute myelogenous leukemia cell (OCI/AML-2) sublines. Paraquat 86-94 RUNX family transcription factor 3 Homo sapiens 147-152 10774745-2 2000 For this, PQ-resistant AML sublines, AML-2/PQ100 and AML-2/PQ400, were selected in the presence of PQ concentrations of 100 microg/ml and 400 microg/ml, respectively. Paraquat 10-12 RUNX family transcription factor 3 Homo sapiens 37-42 10774745-4 2000 They were also slightly more resistant than the parental cell (AML-2/WT) to etoposide, camptothecin and daunorubicin. Camptothecin 87-99 RUNX family transcription factor 3 Homo sapiens 63-68 10774745-2 2000 For this, PQ-resistant AML sublines, AML-2/PQ100 and AML-2/PQ400, were selected in the presence of PQ concentrations of 100 microg/ml and 400 microg/ml, respectively. Paraquat 10-12 RUNX family transcription factor 3 Homo sapiens 53-58 10774745-4 2000 They were also slightly more resistant than the parental cell (AML-2/WT) to etoposide, camptothecin and daunorubicin. Daunorubicin 104-116 RUNX family transcription factor 3 Homo sapiens 63-68 10774745-5 2000 The resistance of PQ-resistant AML-2 sublines to cisplatin seemed to be due to increased amounts of metallothionein, which was not only supported by reversal of resistance to cisplatin by propargylglycin (an inhibitor of metallothionein synthesis) but also confirmed by Western blot analysis and reverse transcription-PCR assay. Paraquat 18-20 RUNX family transcription factor 3 Homo sapiens 31-36 10774745-5 2000 The resistance of PQ-resistant AML-2 sublines to cisplatin seemed to be due to increased amounts of metallothionein, which was not only supported by reversal of resistance to cisplatin by propargylglycin (an inhibitor of metallothionein synthesis) but also confirmed by Western blot analysis and reverse transcription-PCR assay. Cisplatin 49-58 RUNX family transcription factor 3 Homo sapiens 31-36 10774745-5 2000 The resistance of PQ-resistant AML-2 sublines to cisplatin seemed to be due to increased amounts of metallothionein, which was not only supported by reversal of resistance to cisplatin by propargylglycin (an inhibitor of metallothionein synthesis) but also confirmed by Western blot analysis and reverse transcription-PCR assay. Cisplatin 175-184 RUNX family transcription factor 3 Homo sapiens 31-36 10774745-5 2000 The resistance of PQ-resistant AML-2 sublines to cisplatin seemed to be due to increased amounts of metallothionein, which was not only supported by reversal of resistance to cisplatin by propargylglycin (an inhibitor of metallothionein synthesis) but also confirmed by Western blot analysis and reverse transcription-PCR assay. propargylglycin 188-203 RUNX family transcription factor 3 Homo sapiens 31-36 10420992-2 1999 In this study, we investigate which protein is preferentially overexpressed in the function of doxorubicin concentrations in the acute myelogenous leukemia cell line (OCI/AML-2). Doxorubicin 95-106 RUNX family transcription factor 3 Homo sapiens 171-176 10419474-4 1999 In HL-60 cells AML2 expression can be induced by all three natural retinoids, all-trans-retinoic acid (RA), 13-cis-RA, and 9-cis-RA in a dose-dependent manner. Retinoids 67-76 RUNX family transcription factor 3 Homo sapiens 15-19 10419474-4 1999 In HL-60 cells AML2 expression can be induced by all three natural retinoids, all-trans-retinoic acid (RA), 13-cis-RA, and 9-cis-RA in a dose-dependent manner. Tretinoin 78-101 RUNX family transcription factor 3 Homo sapiens 15-19 10419474-4 1999 In HL-60 cells AML2 expression can be induced by all three natural retinoids, all-trans-retinoic acid (RA), 13-cis-RA, and 9-cis-RA in a dose-dependent manner. Tretinoin 103-105 RUNX family transcription factor 3 Homo sapiens 15-19 10419474-4 1999 In HL-60 cells AML2 expression can be induced by all three natural retinoids, all-trans-retinoic acid (RA), 13-cis-RA, and 9-cis-RA in a dose-dependent manner. 13-cis-ra 108-117 RUNX family transcription factor 3 Homo sapiens 15-19 10419474-4 1999 In HL-60 cells AML2 expression can be induced by all three natural retinoids, all-trans-retinoic acid (RA), 13-cis-RA, and 9-cis-RA in a dose-dependent manner. Tretinoin 115-117 RUNX family transcription factor 3 Homo sapiens 15-19 10419474-7 1999 Our study further showed that AGN193109, a potent RARalpha antagonist, suppressed AML2 expression induced by RA and that a retinoic X receptor pan agonist AGN194204 had no effect on its expression. AGN 193109 30-39 RUNX family transcription factor 3 Homo sapiens 82-86 10419474-7 1999 Our study further showed that AGN193109, a potent RARalpha antagonist, suppressed AML2 expression induced by RA and that a retinoic X receptor pan agonist AGN194204 had no effect on its expression. Tretinoin 50-52 RUNX family transcription factor 3 Homo sapiens 82-86 10419474-9 1999 Our study further showed that after all-trans-retinoic acid priming, AML2 expression could be augmented by vitamin D(3). Vitamin D 107-116 RUNX family transcription factor 3 Homo sapiens 69-73 10420992-3 1999 Multidrug-resistant AML-2 sublines were isolated in doxorubicin concentrations of 20, 100, 250, and 500 ng/ml. Doxorubicin 52-63 RUNX family transcription factor 3 Homo sapiens 20-25 9180915-3 1997 A case of AML-2 with t(8;21) and t(3;15) occurring 4 years after treatment for an Ewing"s sarcoma with cyclophosphamide, doxorubicin, vincristine, dactinomycin, and radiotherapy, is reported. Cyclophosphamide 103-119 RUNX family transcription factor 3 Homo sapiens 10-15 9180915-3 1997 A case of AML-2 with t(8;21) and t(3;15) occurring 4 years after treatment for an Ewing"s sarcoma with cyclophosphamide, doxorubicin, vincristine, dactinomycin, and radiotherapy, is reported. Doxorubicin 121-132 RUNX family transcription factor 3 Homo sapiens 10-15 9180915-3 1997 A case of AML-2 with t(8;21) and t(3;15) occurring 4 years after treatment for an Ewing"s sarcoma with cyclophosphamide, doxorubicin, vincristine, dactinomycin, and radiotherapy, is reported. Dactinomycin 147-159 RUNX family transcription factor 3 Homo sapiens 10-15 7807996-13 1994 OCI/AML-2 cells treated with HC before drug accumulated fewer cells with nicked DNA after daunorubicin (DNR). Daunorubicin 90-102 RUNX family transcription factor 3 Homo sapiens 4-9 9207471-4 1997 In cultured OCI/AML-2 myeloblasts and CCRF-CEM T-lymphoblasts, and in fresh leukemic blasts, es sites were fractionally blocked by treatment with graded concentrations of nitrobenzylthioinosine (NBMPR), an inhibitory es site ligand, to simulate the variation in es expression found in leukemic blasts from patients with acute myeloid leukemia. 4-nitrobenzylthioinosine 171-193 RUNX family transcription factor 3 Homo sapiens 16-21 9163728-0 1997 Isolation and characterization of daunorubicin-resistant AML-2 sublines. Daunorubicin 34-46 RUNX family transcription factor 3 Homo sapiens 57-62 9163728-1 1997 An attempt was made to isolate resistant sublines of acute myelogenous leukemia (OCI/ AML-2) cells by chronic exposure to gradually increasing concentrations of daunorubicin in order to determine the mechanism of its resistance to this drug. Daunorubicin 161-173 RUNX family transcription factor 3 Homo sapiens 86-91 9163728-4 1997 The daunorubicin-resistant AML-2 sublines also showed cross resistance to various anticancer drugs including another anthracycline doxorubicin, a Vinca alkaloid vincristine, and an epipodophyllotoxin etoposide. Daunorubicin 4-16 RUNX family transcription factor 3 Homo sapiens 27-32 9163728-4 1997 The daunorubicin-resistant AML-2 sublines also showed cross resistance to various anticancer drugs including another anthracycline doxorubicin, a Vinca alkaloid vincristine, and an epipodophyllotoxin etoposide. Anthracyclines 117-130 RUNX family transcription factor 3 Homo sapiens 27-32 9163728-4 1997 The daunorubicin-resistant AML-2 sublines also showed cross resistance to various anticancer drugs including another anthracycline doxorubicin, a Vinca alkaloid vincristine, and an epipodophyllotoxin etoposide. Doxorubicin 131-142 RUNX family transcription factor 3 Homo sapiens 27-32 9163728-4 1997 The daunorubicin-resistant AML-2 sublines also showed cross resistance to various anticancer drugs including another anthracycline doxorubicin, a Vinca alkaloid vincristine, and an epipodophyllotoxin etoposide. Vinca Alkaloids 146-160 RUNX family transcription factor 3 Homo sapiens 27-32 9163728-4 1997 The daunorubicin-resistant AML-2 sublines also showed cross resistance to various anticancer drugs including another anthracycline doxorubicin, a Vinca alkaloid vincristine, and an epipodophyllotoxin etoposide. Vincristine 161-172 RUNX family transcription factor 3 Homo sapiens 27-32 9163728-4 1997 The daunorubicin-resistant AML-2 sublines also showed cross resistance to various anticancer drugs including another anthracycline doxorubicin, a Vinca alkaloid vincristine, and an epipodophyllotoxin etoposide. epipodophyllotoxin etoposide 181-209 RUNX family transcription factor 3 Homo sapiens 27-32 9163728-5 1997 A functional assay using flow cytometry showed decreased accumulation of daunorubicin in these sublines as compared to that of AML-2, which was reversed by cyclosporin A or cyanide. Cyclosporine 156-169 RUNX family transcription factor 3 Homo sapiens 127-132 9163728-5 1997 A functional assay using flow cytometry showed decreased accumulation of daunorubicin in these sublines as compared to that of AML-2, which was reversed by cyclosporin A or cyanide. Cyanides 173-180 RUNX family transcription factor 3 Homo sapiens 127-132 9163728-10 1997 These daunorubicin-resistant AML-2 sublines could provide a useful model for the study of multidrug resistance mediated by PGP. Daunorubicin 6-18 RUNX family transcription factor 3 Homo sapiens 29-34 7769841-4 1995 Exposure of OCI/AML-2 or OCI/AML-5 cells to retinoic acid (all-trans retinoic acid, ATRA) led to a down-regulation of bcl-2 expression that was first seen after 2 h of exposure and was complete after a day. Tretinoin 44-57 RUNX family transcription factor 3 Homo sapiens 16-21 7769841-4 1995 Exposure of OCI/AML-2 or OCI/AML-5 cells to retinoic acid (all-trans retinoic acid, ATRA) led to a down-regulation of bcl-2 expression that was first seen after 2 h of exposure and was complete after a day. Tretinoin 59-82 RUNX family transcription factor 3 Homo sapiens 16-21 7769841-4 1995 Exposure of OCI/AML-2 or OCI/AML-5 cells to retinoic acid (all-trans retinoic acid, ATRA) led to a down-regulation of bcl-2 expression that was first seen after 2 h of exposure and was complete after a day. Tretinoin 84-88 RUNX family transcription factor 3 Homo sapiens 16-21 34719421-13 2021 MiR-138 could target the expression of RUNX3. mir-138 0-7 RUNX family transcription factor 3 Homo sapiens 39-44 31308194-7 2019 Treatment with RUNX3 siRNA attenuates VPA-induced RUNX3 elevation and TrkB downregulation. Valproic Acid 38-41 RUNX family transcription factor 3 Homo sapiens 15-20 31308194-7 2019 Treatment with RUNX3 siRNA attenuates VPA-induced RUNX3 elevation and TrkB downregulation. Valproic Acid 38-41 RUNX family transcription factor 3 Homo sapiens 50-55 31308194-8 2019 VPA, entinostat, HDAC1 depletion by siRNA, and 3-deazaneplanocin A (DZNep), an inhibitor of the polycomb repressor complex 2 (PRC2), decrease the PRC2 core component EZH2, a RUNX3 suppressor. 3-deazaneplanocin 47-66 RUNX family transcription factor 3 Homo sapiens 174-179 31308194-8 2019 VPA, entinostat, HDAC1 depletion by siRNA, and 3-deazaneplanocin A (DZNep), an inhibitor of the polycomb repressor complex 2 (PRC2), decrease the PRC2 core component EZH2, a RUNX3 suppressor. 3-deazaneplanocin 68-73 RUNX family transcription factor 3 Homo sapiens 174-179 34980322-1 2021 Objective To investigate the expression and correlation of Runt-related transcription factor 3(RUNX3)and enhancer of zeste homolog 2(EZH2)in rectal cancer,and to reveal the relationship between the expression of RUNX3 and EZH2 and the sensitivity of XELOX regimen to neoadjuvant chemotherapy in locally advanced rectal cancer patients. XELOX 250-255 RUNX family transcription factor 3 Homo sapiens 59-94 34980322-1 2021 Objective To investigate the expression and correlation of Runt-related transcription factor 3(RUNX3)and enhancer of zeste homolog 2(EZH2)in rectal cancer,and to reveal the relationship between the expression of RUNX3 and EZH2 and the sensitivity of XELOX regimen to neoadjuvant chemotherapy in locally advanced rectal cancer patients. XELOX 250-255 RUNX family transcription factor 3 Homo sapiens 95-100 34980322-1 2021 Objective To investigate the expression and correlation of Runt-related transcription factor 3(RUNX3)and enhancer of zeste homolog 2(EZH2)in rectal cancer,and to reveal the relationship between the expression of RUNX3 and EZH2 and the sensitivity of XELOX regimen to neoadjuvant chemotherapy in locally advanced rectal cancer patients. XELOX 250-255 RUNX family transcription factor 3 Homo sapiens 212-217 34980322-4 2021 Conclusions The positive expression rate of RUNX3 in cancer tissue was lower than that in paracancerous tissue,while that of EZH2 showed the opposite trend.Neoadjuvant chemotherapy may affect the expression of RUNX3 and EZH2 in rectal cancer.The patients with high RUNX3 expression and low EZH2 expression in locally advanced rectal cancer were more sensitive to neoadjuvant chemotherapy with XELOX regimen. XELOX 393-398 RUNX family transcription factor 3 Homo sapiens 44-49 34980322-4 2021 Conclusions The positive expression rate of RUNX3 in cancer tissue was lower than that in paracancerous tissue,while that of EZH2 showed the opposite trend.Neoadjuvant chemotherapy may affect the expression of RUNX3 and EZH2 in rectal cancer.The patients with high RUNX3 expression and low EZH2 expression in locally advanced rectal cancer were more sensitive to neoadjuvant chemotherapy with XELOX regimen. XELOX 393-398 RUNX family transcription factor 3 Homo sapiens 210-215 34980322-4 2021 Conclusions The positive expression rate of RUNX3 in cancer tissue was lower than that in paracancerous tissue,while that of EZH2 showed the opposite trend.Neoadjuvant chemotherapy may affect the expression of RUNX3 and EZH2 in rectal cancer.The patients with high RUNX3 expression and low EZH2 expression in locally advanced rectal cancer were more sensitive to neoadjuvant chemotherapy with XELOX regimen. XELOX 393-398 RUNX family transcription factor 3 Homo sapiens 265-270 34611951-11 2021 Finally, we showed that Runx3 enhanced the activity of the BMP6 promoter by responding to iron stimuli in the hepatocytes. Iron 90-94 RUNX family transcription factor 3 Homo sapiens 24-29 34611951-12 2021 CONCLUSION: In conclusion, we suggest that Runx3 plays important roles in iron metabolism of the liver through regulation of BMP signalling. Iron 74-78 RUNX family transcription factor 3 Homo sapiens 43-48 34681943-9 2021 These effects are mediated via ROS generation and changes in gene expression, including upregulation of Wnt/beta-catenin pathway antagonists, SFRP1, and RUNX3, and downregulation of UHRF1, the key epigenetic regulator. Reactive Oxygen Species 31-34 RUNX family transcription factor 3 Homo sapiens 153-158 34719421-15 2021 CONCLUSIONS: MiR-138 regulates Th1/Th2 balance by targeting RUNX3 in children with CVA, providing a new direction for the treatment of CVA. mir-138 13-20 RUNX family transcription factor 3 Homo sapiens 60-65 34728031-1 2021 Objective To establish a human colon cancer cell line HCT-116/5-FU resistant to 5-fluorouracil(5-FU)and explore the relationship between runt-related transcription factor 3(RUNX3)and drug resistance of colorectal cancer.Methods The human colon cancer cell line HCT-116/5-FU with resistance to 5-FU was established by low concentration gradient increment combined with high-dose intermittent shock.CCK-8 method was used to determine the half maximal inhibitory concentration(IC50)of 5-FU on the parent line HCT-116 and drug-resistant line HCT-116/5-FU.The cell growth curve was established for the calculation of population doubling time(TD).The mRNA levels and protein levels of RUNX3,P-glycoprotein(P-gp),multidrug resistance-associated protein 1(MRP1),and lung resistance-related protein(LRP)in HCT-116 and HCT-116/5-FU cells were determined by qRT-PCR and Western blotting,respectively.The RUNX3 expression in HCT-116 cells was knocked down by siRNA technique,and the cells were divided into RUNX3 knockdown groups(si-RUNX3-1 group and si-RUNX3-2 group)and negative control group(si-NC group).The knockdown efficiency was verified by qRT-PCR at the mRNA level and Western blotting at the protein level.The IC50 in si-RUNX3 groups and si-NC group was determined with CCK-8 method,and the expression of P-gp,MRP1,and LRP in the two groups was detected by Western blotting.Results A stable human colon cancer drug-resistant cell line HCT-116/5-FU was successfully constructed.HCT-116/5-FU showed the TD 1.38 times as long as that of HCT-116(P=0.002)and changed morphology.The mRNA level of RUNX3 in HCT-116/5-FU cells was significantly lower than that in HCT-116 cells(P=0.048),and those of P-gp(P=0.008),MRP1(P=0.001),and LRP(P=0.001)showed the opposite trend.The protein level of RUNX3 in HCT-116/5-FU cells was significantly lower than that in HCT-116(P<0.001),and those of P-gp,MRP1,and LRP presented the opposite trend(all P<0.001).The HCT-116 cell model with low expression of RUNX3 was successfully established.The mRNA level of RUNX3 had no significant difference between si-RUNX3-1 group and si-NC group(P=0.064),while the level in si-RUNX3-2 group was significantly lower than that in si-NC group(P=0.034).The protein levels of RUNX3 in si-RUNX3-1 group and si-RUNX3-2 group were lower than that in si-NC group(both P<0.001).The results demonstrated higher knocking efficiency in si-RUNX3-2 group,which was thus selected to complete the follow-up test.The IC50 of si-RUNX3 group was significantly higher than that of si-NC group(P<0.001),which indicated that the down-regulated expression of RUNX3 could reduce the sensitivity of HCT-116 cells to 5-FU.The relative protein levels of P-gp,MRP1,and LRP in si-RUNX3 group were significantly higher than those in si-NC group(all P<0.001).Conclusion The down-regulation of RUNX3 expression can reduce the sensitivity of HCT-116 cells to 5-FU,which is considered to be related to the up-regulated expression of P-gp,MRP1,and LRP. Fluorouracil 269-273 RUNX family transcription factor 3 Homo sapiens 137-172 34728031-0 2021 (Expression of Runt-related Transcription Factor 3 in Human Colon Cancer Cell Line HCT-116 Resistant to 5-Fluorouracil and the Mechanism of Drug Resistance). Fluorouracil 104-118 RUNX family transcription factor 3 Homo sapiens 15-50 34728031-1 2021 Objective To establish a human colon cancer cell line HCT-116/5-FU resistant to 5-fluorouracil(5-FU)and explore the relationship between runt-related transcription factor 3(RUNX3)and drug resistance of colorectal cancer.Methods The human colon cancer cell line HCT-116/5-FU with resistance to 5-FU was established by low concentration gradient increment combined with high-dose intermittent shock.CCK-8 method was used to determine the half maximal inhibitory concentration(IC50)of 5-FU on the parent line HCT-116 and drug-resistant line HCT-116/5-FU.The cell growth curve was established for the calculation of population doubling time(TD).The mRNA levels and protein levels of RUNX3,P-glycoprotein(P-gp),multidrug resistance-associated protein 1(MRP1),and lung resistance-related protein(LRP)in HCT-116 and HCT-116/5-FU cells were determined by qRT-PCR and Western blotting,respectively.The RUNX3 expression in HCT-116 cells was knocked down by siRNA technique,and the cells were divided into RUNX3 knockdown groups(si-RUNX3-1 group and si-RUNX3-2 group)and negative control group(si-NC group).The knockdown efficiency was verified by qRT-PCR at the mRNA level and Western blotting at the protein level.The IC50 in si-RUNX3 groups and si-NC group was determined with CCK-8 method,and the expression of P-gp,MRP1,and LRP in the two groups was detected by Western blotting.Results A stable human colon cancer drug-resistant cell line HCT-116/5-FU was successfully constructed.HCT-116/5-FU showed the TD 1.38 times as long as that of HCT-116(P=0.002)and changed morphology.The mRNA level of RUNX3 in HCT-116/5-FU cells was significantly lower than that in HCT-116 cells(P=0.048),and those of P-gp(P=0.008),MRP1(P=0.001),and LRP(P=0.001)showed the opposite trend.The protein level of RUNX3 in HCT-116/5-FU cells was significantly lower than that in HCT-116(P<0.001),and those of P-gp,MRP1,and LRP presented the opposite trend(all P<0.001).The HCT-116 cell model with low expression of RUNX3 was successfully established.The mRNA level of RUNX3 had no significant difference between si-RUNX3-1 group and si-NC group(P=0.064),while the level in si-RUNX3-2 group was significantly lower than that in si-NC group(P=0.034).The protein levels of RUNX3 in si-RUNX3-1 group and si-RUNX3-2 group were lower than that in si-NC group(both P<0.001).The results demonstrated higher knocking efficiency in si-RUNX3-2 group,which was thus selected to complete the follow-up test.The IC50 of si-RUNX3 group was significantly higher than that of si-NC group(P<0.001),which indicated that the down-regulated expression of RUNX3 could reduce the sensitivity of HCT-116 cells to 5-FU.The relative protein levels of P-gp,MRP1,and LRP in si-RUNX3 group were significantly higher than those in si-NC group(all P<0.001).Conclusion The down-regulation of RUNX3 expression can reduce the sensitivity of HCT-116 cells to 5-FU,which is considered to be related to the up-regulated expression of P-gp,MRP1,and LRP. Fluorouracil 293-297 RUNX family transcription factor 3 Homo sapiens 137-172 34728031-1 2021 Objective To establish a human colon cancer cell line HCT-116/5-FU resistant to 5-fluorouracil(5-FU)and explore the relationship between runt-related transcription factor 3(RUNX3)and drug resistance of colorectal cancer.Methods The human colon cancer cell line HCT-116/5-FU with resistance to 5-FU was established by low concentration gradient increment combined with high-dose intermittent shock.CCK-8 method was used to determine the half maximal inhibitory concentration(IC50)of 5-FU on the parent line HCT-116 and drug-resistant line HCT-116/5-FU.The cell growth curve was established for the calculation of population doubling time(TD).The mRNA levels and protein levels of RUNX3,P-glycoprotein(P-gp),multidrug resistance-associated protein 1(MRP1),and lung resistance-related protein(LRP)in HCT-116 and HCT-116/5-FU cells were determined by qRT-PCR and Western blotting,respectively.The RUNX3 expression in HCT-116 cells was knocked down by siRNA technique,and the cells were divided into RUNX3 knockdown groups(si-RUNX3-1 group and si-RUNX3-2 group)and negative control group(si-NC group).The knockdown efficiency was verified by qRT-PCR at the mRNA level and Western blotting at the protein level.The IC50 in si-RUNX3 groups and si-NC group was determined with CCK-8 method,and the expression of P-gp,MRP1,and LRP in the two groups was detected by Western blotting.Results A stable human colon cancer drug-resistant cell line HCT-116/5-FU was successfully constructed.HCT-116/5-FU showed the TD 1.38 times as long as that of HCT-116(P=0.002)and changed morphology.The mRNA level of RUNX3 in HCT-116/5-FU cells was significantly lower than that in HCT-116 cells(P=0.048),and those of P-gp(P=0.008),MRP1(P=0.001),and LRP(P=0.001)showed the opposite trend.The protein level of RUNX3 in HCT-116/5-FU cells was significantly lower than that in HCT-116(P<0.001),and those of P-gp,MRP1,and LRP presented the opposite trend(all P<0.001).The HCT-116 cell model with low expression of RUNX3 was successfully established.The mRNA level of RUNX3 had no significant difference between si-RUNX3-1 group and si-NC group(P=0.064),while the level in si-RUNX3-2 group was significantly lower than that in si-NC group(P=0.034).The protein levels of RUNX3 in si-RUNX3-1 group and si-RUNX3-2 group were lower than that in si-NC group(both P<0.001).The results demonstrated higher knocking efficiency in si-RUNX3-2 group,which was thus selected to complete the follow-up test.The IC50 of si-RUNX3 group was significantly higher than that of si-NC group(P<0.001),which indicated that the down-regulated expression of RUNX3 could reduce the sensitivity of HCT-116 cells to 5-FU.The relative protein levels of P-gp,MRP1,and LRP in si-RUNX3 group were significantly higher than those in si-NC group(all P<0.001).Conclusion The down-regulation of RUNX3 expression can reduce the sensitivity of HCT-116 cells to 5-FU,which is considered to be related to the up-regulated expression of P-gp,MRP1,and LRP. Fluorouracil 293-297 RUNX family transcription factor 3 Homo sapiens 173-178 34082012-4 2021 The functions of YBX1, miR-148a-3p and Runx3 were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, colony formation, wound healing, transwell, flow cytometry, xenograft model and Western blotting analyses. thiazolyl blue 62-122 RUNX family transcription factor 3 Homo sapiens 39-44 34397122-2 2022 In this study, we identified AYNE as the most potent FAO inhibitor within the Avo-B mixture capable of inducing cell death in leukemia cells lines (IC50 : 3.10 +- 0.14 microM in TEX cells; 11.53 +- 3.32 microM in OCI-AML2) and patient-derived acute myeloid leukemia cells. ayne 29-33 RUNX family transcription factor 3 Homo sapiens 217-221 34397327-10 2021 GSEA showed that RUNX3 expression was positively correlated with melanogenesis and melanoma pathways. gsea 0-4 RUNX family transcription factor 3 Homo sapiens 17-22 34799276-8 2022 Following intervention with oestrogen, it was observed that the oestradiol group showed higher levels of RUNX3 methylation (P < 0.001) and DNA methyltransferase 1 (DNMT1) mRNA and protein expression (P < 0.001 and P < 0.001), and lower RUNX3 mRNA and protein expression when compared with the ESC group (P < 0.001 and P < 0.001). Estradiol 64-74 RUNX family transcription factor 3 Homo sapiens 105-110 34253860-7 2021 We also tested the efficacy of this peptide to block the RUNX3 Threonine 209 phosphorylation mediated tumorigenic functions in in vitro cell culture models, patient-derived explant (PDE) models and in in vivo tumor xenograft models. Threonine 63-72 RUNX family transcription factor 3 Homo sapiens 57-62 34253860-8 2021 These results proved that this peptide has the potential to be developed as an efficient therapeutic molecule for targeting RUNX3 Threonine 209 phosphorylation-dependent tumor phenotypes. Threonine 130-139 RUNX family transcription factor 3 Homo sapiens 124-129 34253860-3 2021 Previous findings from our laboratory provided evidence that Threonine 209 phosphorylation of RUNX3 acts as a molecular switch in dictating the tissue-specific dualistic functions of RUNX3 for the first time. Threonine 61-70 RUNX family transcription factor 3 Homo sapiens 94-99 34253860-3 2021 Previous findings from our laboratory provided evidence that Threonine 209 phosphorylation of RUNX3 acts as a molecular switch in dictating the tissue-specific dualistic functions of RUNX3 for the first time. Threonine 61-70 RUNX family transcription factor 3 Homo sapiens 183-188 34253860-4 2021 Based on these proofs and to explore the translational significance of these findings, we designed a small peptide (RMR) from the protein sequence of RUNX3 flanking the Threonine 209 phosphorylation site. Threonine 169-178 RUNX family transcription factor 3 Homo sapiens 150-155 34253860-6 2021 We found that this peptide is stable both in in vitro and in vivo conditions, not toxic to normal cells and inhibits the Threonine 209 phosphorylation in RUNX3 by PAK1. Threonine 121-130 RUNX family transcription factor 3 Homo sapiens 154-159 34799276-8 2022 Following intervention with oestrogen, it was observed that the oestradiol group showed higher levels of RUNX3 methylation (P < 0.001) and DNA methyltransferase 1 (DNMT1) mRNA and protein expression (P < 0.001 and P < 0.001), and lower RUNX3 mRNA and protein expression when compared with the ESC group (P < 0.001 and P < 0.001). Estradiol 64-74 RUNX family transcription factor 3 Homo sapiens 236-241 34360553-7 2021 TrkC upregulation by VPA involved induction of RUNX3, stimulation of ERK1/2 and JNK, and ERK1/2-mediated Egr1 expression. Valproic Acid 21-24 RUNX family transcription factor 3 Homo sapiens 47-52 35527485-6 2022 The changes in GSH/GSSG and NADPH/NADP ratios in NCI N87R/RUNX3 cells were measured using detection kits. NADP 28-33 RUNX family transcription factor 3 Homo sapiens 58-63 35527485-6 2022 The changes in GSH/GSSG and NADPH/NADP ratios in NCI N87R/RUNX3 cells were measured using detection kits. NADP 34-38 RUNX family transcription factor 3 Homo sapiens 58-63 35527485-8 2022 In NCI N87R cells, RUNX3 knockdown resulted in noticeable alterations in 8 pathways involving glutamine metabolism, glycolysis, glycerophospholipid, nicotinate-nicotinamide and glutathione metabolism, causing also significant reduction of intracellular GSH/GSSG and NADPH/NADP ratios (P < 0.01). Glutamine 94-103 RUNX family transcription factor 3 Homo sapiens 19-24 35527485-8 2022 In NCI N87R cells, RUNX3 knockdown resulted in noticeable alterations in 8 pathways involving glutamine metabolism, glycolysis, glycerophospholipid, nicotinate-nicotinamide and glutathione metabolism, causing also significant reduction of intracellular GSH/GSSG and NADPH/NADP ratios (P < 0.01). Glycerophospholipids 128-147 RUNX family transcription factor 3 Homo sapiens 19-24 35527485-8 2022 In NCI N87R cells, RUNX3 knockdown resulted in noticeable alterations in 8 pathways involving glutamine metabolism, glycolysis, glycerophospholipid, nicotinate-nicotinamide and glutathione metabolism, causing also significant reduction of intracellular GSH/GSSG and NADPH/NADP ratios (P < 0.01). Niacin 149-159 RUNX family transcription factor 3 Homo sapiens 19-24 35527485-8 2022 In NCI N87R cells, RUNX3 knockdown resulted in noticeable alterations in 8 pathways involving glutamine metabolism, glycolysis, glycerophospholipid, nicotinate-nicotinamide and glutathione metabolism, causing also significant reduction of intracellular GSH/GSSG and NADPH/NADP ratios (P < 0.01). Niacinamide 160-172 RUNX family transcription factor 3 Homo sapiens 19-24 35527485-8 2022 In NCI N87R cells, RUNX3 knockdown resulted in noticeable alterations in 8 pathways involving glutamine metabolism, glycolysis, glycerophospholipid, nicotinate-nicotinamide and glutathione metabolism, causing also significant reduction of intracellular GSH/GSSG and NADPH/NADP ratios (P < 0.01). Glutathione 177-188 RUNX family transcription factor 3 Homo sapiens 19-24 35527485-8 2022 In NCI N87R cells, RUNX3 knockdown resulted in noticeable alterations in 8 pathways involving glutamine metabolism, glycolysis, glycerophospholipid, nicotinate-nicotinamide and glutathione metabolism, causing also significant reduction of intracellular GSH/GSSG and NADPH/NADP ratios (P < 0.01). Glutathione 253-256 RUNX family transcription factor 3 Homo sapiens 19-24 35527485-8 2022 In NCI N87R cells, RUNX3 knockdown resulted in noticeable alterations in 8 pathways involving glutamine metabolism, glycolysis, glycerophospholipid, nicotinate-nicotinamide and glutathione metabolism, causing also significant reduction of intracellular GSH/GSSG and NADPH/NADP ratios (P < 0.01). Glutathione Disulfide 257-261 RUNX family transcription factor 3 Homo sapiens 19-24 35527485-8 2022 In NCI N87R cells, RUNX3 knockdown resulted in noticeable alterations in 8 pathways involving glutamine metabolism, glycolysis, glycerophospholipid, nicotinate-nicotinamide and glutathione metabolism, causing also significant reduction of intracellular GSH/GSSG and NADPH/NADP ratios (P < 0.01). NADP 266-271 RUNX family transcription factor 3 Homo sapiens 19-24 35527485-8 2022 In NCI N87R cells, RUNX3 knockdown resulted in noticeable alterations in 8 pathways involving glutamine metabolism, glycolysis, glycerophospholipid, nicotinate-nicotinamide and glutathione metabolism, causing also significant reduction of intracellular GSH/GSSG and NADPH/NADP ratios (P < 0.01). NADP 272-276 RUNX family transcription factor 3 Homo sapiens 19-24