PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 34275467-7 2021 Notably, the mTOR activator MHY1485 rescued the inhibitory effect of miR-34b. 4,6-dimorpholino-N-(4-nitrophenyl)-1,3,5-triazin-2-amine 28-35 microRNA 34b Homo sapiens 69-76 34837933-8 2021 We found that treatment with 5-AZA could increase the expression of epigenetically silenced miRNAs, miR-34a, miR-34b and miR-124-1 in treated cells. Azacitidine 29-34 microRNA 34b Homo sapiens 109-116 34045473-10 2021 In summary, the data of this study showed that minor allele (A) of rs55763075 polymorphisms in the 3"-untranslated region of MTHFR mRNA generated a potential binding site for miR-34b, which led to reduced level of folic acid in the patients carrying the AA genotype. Folic Acid 214-224 microRNA 34b Homo sapiens 175-182 35079080-8 2022 Down-regulated miR-34b/c expression was associated with smoking (p = 0.047), alcohol use (p = 0.009), stage (p = 0.025), recurrences (p = 0.000), and a poor survival (p = 0.00029). Alcohols 77-84 microRNA 34b Homo sapiens 15-24 35367965-0 2022 Early-Life Pb Exposure Might Exert Synapse-Toxic Effects Via Inhibiting Synapse-Associated Membrane Protein 2 (VAMP2) Mediated by Upregulation of miR-34b. Lead 11-13 microRNA 34b Homo sapiens 146-153 31870133-9 2020 Additionally, miR-34b induced by nutlin-3 directly targeted the coding sequences (CDS) of NIK. nutlin 3 33-41 microRNA 34b Homo sapiens 14-21 33300049-0 2020 MicroRNA-34b expression enhances chemosensitivity of endometrial cancer cells to paclitaxel. Paclitaxel 81-91 microRNA 34b Homo sapiens 0-12 33300049-7 2020 Sensitivity to paclitaxel was increased in cancer cells with miR-34b overexpression, compared with untreated cancer cells, but this difference was not identified for cisplatin or doxorubicin. Paclitaxel 15-25 microRNA 34b Homo sapiens 61-68 33300049-8 2020 In vivo, combination treatment with miR-34b and paclitaxel markedly reduced tumor growth compared with treatment with negative control miRNA and paclitaxel. Paclitaxel 145-155 microRNA 34b Homo sapiens 36-43 33300049-9 2020 These data suggest that miR-34b enhances paclitaxel sensitivity in endometrial cancer cells, and that miR-34b and MET are key targets for treatment of endometrial cancer. Paclitaxel 41-51 microRNA 34b Homo sapiens 24-31 32149930-7 2020 Further analysis demonstrated that the expression levels of miR-34b and miR-34c were also downregulated in the individuals carrying rs4938723 CC genotype by contrast with that carrying TT + TC genotypes (P < 0.05). tt + tc 185-192 microRNA 34b Homo sapiens 60-67 31665127-4 2019 MATERIAL AND METHODS Expression of miR-34b, IL-6R, and other key factors of inflammation, apoptosis (TNF-alpha, IL-1ss, IL-6, caspase-3) in high glucose (HG)-induced HK-2 cells were measured by real-time PCR, Western blot, and flow cytometric cell apoptosis assays. Glucose 145-152 microRNA 34b Homo sapiens 35-42 31827397-0 2019 Exosomal lncRNA HNF1A-AS1 affects cisplatin resistance in cervical cancer cells through regulating microRNA-34b/TUFT1 axis. Cisplatin 34-43 microRNA 34b Homo sapiens 99-111 31827397-14 2019 Conclusion: Our study provides evidence that CC-secreted exosomes carrying HNF1A-AS1 as a ceRNA of miR-34b to promote the expression of TUFT1, thereby promoting the DDP resistance in CC cells. 2-dimethylaminoethyl(dimethylamido)phosphonofluoridate 165-168 microRNA 34b Homo sapiens 99-106 31325764-7 2019 We found that both TP53 Arg72Pro (CG/GG vs. CC: adjusted OR = 0.82, 95% CI = 0.69-0.98) and miR-34b/c rs4938723 (TC/CC vs. TT: adjusted OR = 0.64, 95% CI = 0.54-0.75) were associated with decreased neuroblastoma susceptibility. Technetium 113-115 microRNA 34b Homo sapiens 92-99 27503378-0 2016 MicroRNA-34b/c inhibits aldosterone-induced vascular smooth muscle cell calcification via a SATB2/Runx2 pathway. Aldosterone 24-35 microRNA 34b Homo sapiens 0-12 31934154-4 2019 Our results showed that the overall average methylation levels of miR-34b/c were significantly higher in the ESCC samples than they were in the ACN and NE samples (P < 0.05). acn 144-147 microRNA 34b Homo sapiens 66-73 31129659-5 2019 Bisulphite sequencing PCR (BSP) uncovered that CpG sites upstream of miR-34b DNA were hypermethylated in calcified VSMCs and calcified arteries due to 5/6 NTP, as well as calcified renal arterial tissues from uraemia patients. hydrogen sulfite 0-10 microRNA 34b Homo sapiens 69-76 31129659-6 2019 Meantime, increased DNA methyltransferase 3a (DNMT3a) resulted in the hypermethylation of miR-34b in VSMCs, while 5-aza-2"-deoxycytidine (5-aza) reduced the methylation rate of miR-34b and restored the expression of miR-34b in VSMCs. Decitabine 114-136 microRNA 34b Homo sapiens 177-184 31129659-6 2019 Meantime, increased DNA methyltransferase 3a (DNMT3a) resulted in the hypermethylation of miR-34b in VSMCs, while 5-aza-2"-deoxycytidine (5-aza) reduced the methylation rate of miR-34b and restored the expression of miR-34b in VSMCs. Decitabine 114-136 microRNA 34b Homo sapiens 177-184 28840508-7 2017 Downregulation of VEGF-A, Bcl-2 and Notch1 proteins in thyroid carcinoma cells were noted in cells that transiently transfected with miR-34b-5p mimic. CHEMBL3740941 141-143 microRNA 34b Homo sapiens 133-140 28690499-8 2017 The correlation between miR-34b and miR-153 expressions was significantly reduced (P < 0.05) in the PD group. mir-153 36-43 microRNA 34b Homo sapiens 24-31 28512015-7 2017 For both miR-34b and miR-34c, a significantly lower expression level was determined in metastasizing LACs compared to non-metastasizing LACs (p=0.0005 and p=0.002) with similarly decreased expression levels observed in the paired distant metastases. Lactose 101-105 microRNA 34b Homo sapiens 9-16 28143614-10 2017 Moreover, higher miR-129-2 independently predicted for shorter DSS and miR-34b/c methylation levels independently predicted for shorter DFS and DSS. dss 144-147 microRNA 34b Homo sapiens 71-78 28039468-9 2017 We found that miR-34b downregulation in African-Americans is inversely correlated with high AR levels that lead to increased cell proliferation. Argon 92-94 microRNA 34b Homo sapiens 14-21 28977792-7 2017 Meanwhile, we also conducted real time PCR and Western blot analysis to study the mRNA and protein expression level of MET1 among different genotypes or cells treated with different concentration of miR-34b mimics/inhibitors, indicating the negative regulatory relationship between miR-34b and MET1.We also investigated the relative viability of EGC cells when transfected with miR-34b mimics (50nM and 100nM) and miR-34b inhibitors (100nM) to validate miR-34b to be negatively interfering with the viability of EGC cells. (-)-Epigallocatechin 346-349 microRNA 34b Homo sapiens 199-206 28977792-7 2017 Meanwhile, we also conducted real time PCR and Western blot analysis to study the mRNA and protein expression level of MET1 among different genotypes or cells treated with different concentration of miR-34b mimics/inhibitors, indicating the negative regulatory relationship between miR-34b and MET1.We also investigated the relative viability of EGC cells when transfected with miR-34b mimics (50nM and 100nM) and miR-34b inhibitors (100nM) to validate miR-34b to be negatively interfering with the viability of EGC cells. (-)-Epigallocatechin 346-349 microRNA 34b Homo sapiens 282-289 28977792-7 2017 Meanwhile, we also conducted real time PCR and Western blot analysis to study the mRNA and protein expression level of MET1 among different genotypes or cells treated with different concentration of miR-34b mimics/inhibitors, indicating the negative regulatory relationship between miR-34b and MET1.We also investigated the relative viability of EGC cells when transfected with miR-34b mimics (50nM and 100nM) and miR-34b inhibitors (100nM) to validate miR-34b to be negatively interfering with the viability of EGC cells. (-)-Epigallocatechin 346-349 microRNA 34b Homo sapiens 282-289 28977792-7 2017 Meanwhile, we also conducted real time PCR and Western blot analysis to study the mRNA and protein expression level of MET1 among different genotypes or cells treated with different concentration of miR-34b mimics/inhibitors, indicating the negative regulatory relationship between miR-34b and MET1.We also investigated the relative viability of EGC cells when transfected with miR-34b mimics (50nM and 100nM) and miR-34b inhibitors (100nM) to validate miR-34b to be negatively interfering with the viability of EGC cells. (-)-Epigallocatechin 346-349 microRNA 34b Homo sapiens 282-289 28977792-7 2017 Meanwhile, we also conducted real time PCR and Western blot analysis to study the mRNA and protein expression level of MET1 among different genotypes or cells treated with different concentration of miR-34b mimics/inhibitors, indicating the negative regulatory relationship between miR-34b and MET1.We also investigated the relative viability of EGC cells when transfected with miR-34b mimics (50nM and 100nM) and miR-34b inhibitors (100nM) to validate miR-34b to be negatively interfering with the viability of EGC cells. (-)-Epigallocatechin 346-349 microRNA 34b Homo sapiens 282-289 28977792-7 2017 Meanwhile, we also conducted real time PCR and Western blot analysis to study the mRNA and protein expression level of MET1 among different genotypes or cells treated with different concentration of miR-34b mimics/inhibitors, indicating the negative regulatory relationship between miR-34b and MET1.We also investigated the relative viability of EGC cells when transfected with miR-34b mimics (50nM and 100nM) and miR-34b inhibitors (100nM) to validate miR-34b to be negatively interfering with the viability of EGC cells. (-)-Epigallocatechin 512-515 microRNA 34b Homo sapiens 199-206 28977792-7 2017 Meanwhile, we also conducted real time PCR and Western blot analysis to study the mRNA and protein expression level of MET1 among different genotypes or cells treated with different concentration of miR-34b mimics/inhibitors, indicating the negative regulatory relationship between miR-34b and MET1.We also investigated the relative viability of EGC cells when transfected with miR-34b mimics (50nM and 100nM) and miR-34b inhibitors (100nM) to validate miR-34b to be negatively interfering with the viability of EGC cells. (-)-Epigallocatechin 512-515 microRNA 34b Homo sapiens 282-289 28977792-7 2017 Meanwhile, we also conducted real time PCR and Western blot analysis to study the mRNA and protein expression level of MET1 among different genotypes or cells treated with different concentration of miR-34b mimics/inhibitors, indicating the negative regulatory relationship between miR-34b and MET1.We also investigated the relative viability of EGC cells when transfected with miR-34b mimics (50nM and 100nM) and miR-34b inhibitors (100nM) to validate miR-34b to be negatively interfering with the viability of EGC cells. (-)-Epigallocatechin 512-515 microRNA 34b Homo sapiens 282-289 28977792-7 2017 Meanwhile, we also conducted real time PCR and Western blot analysis to study the mRNA and protein expression level of MET1 among different genotypes or cells treated with different concentration of miR-34b mimics/inhibitors, indicating the negative regulatory relationship between miR-34b and MET1.We also investigated the relative viability of EGC cells when transfected with miR-34b mimics (50nM and 100nM) and miR-34b inhibitors (100nM) to validate miR-34b to be negatively interfering with the viability of EGC cells. (-)-Epigallocatechin 512-515 microRNA 34b Homo sapiens 282-289 28977792-7 2017 Meanwhile, we also conducted real time PCR and Western blot analysis to study the mRNA and protein expression level of MET1 among different genotypes or cells treated with different concentration of miR-34b mimics/inhibitors, indicating the negative regulatory relationship between miR-34b and MET1.We also investigated the relative viability of EGC cells when transfected with miR-34b mimics (50nM and 100nM) and miR-34b inhibitors (100nM) to validate miR-34b to be negatively interfering with the viability of EGC cells. (-)-Epigallocatechin 512-515 microRNA 34b Homo sapiens 282-289 27503378-2 2016 In this study, we aim to explore the mechanistic links between miR-34b/c and aldosterone in VSMC calcification. Aldosterone 77-88 microRNA 34b Homo sapiens 63-70 27503378-10 2016 Furthermore, miR-34b/c overexpression alleviated aldosterone-induced VSMC calcification as well as inhibited the expression of SATB2 protein, whereas miR-34b/c inhibition markedly enhanced VSMC calcification and upregulated SATB2 protein. Aldosterone 49-60 microRNA 34b Homo sapiens 13-20 27767101-2 2016 Here, we show that oxidative stress (hydrogen peroxide) selectively elevates microRNA-34a (miR-34a) but not the related miR-34b/c, with concomitant reduction of SIRT1/-6 in bronchial epithelial cells (BEAS2B), which was also observed in peripheral lung samples from patients with COPD. Hydrogen Peroxide 37-54 microRNA 34b Homo sapiens 120-127 26924291-11 2016 Treatment of with sirolimus increased miR-34b levels by a factor of 7.5 in the cells. Sirolimus 18-27 microRNA 34b Homo sapiens 38-45 27362652-9 2016 Overexpression of miR-34a, miR-34b, or miR-34c in lung epithelial cells was associated with higher SA-betagal activity (27.8%, 35.1%, and 38.2%, respectively) relative to control treated cells (8.8%). 2-chloro-10-(4'(N-beta-hydroxyethyl)piperazinyl-1')acetylphenothiazine 99-101 microRNA 34b Homo sapiens 27-34 26924291-12 2016 Upregulation of miR-34b also induced apoptosis and increased the sensitivity of the cells to the anticancer drugs, whereas transfection with miR-34b-AMO, an inhibitor of miR-34b, reversed the anti-proliferation effect of sirolimus. Sirolimus 221-230 microRNA 34b Homo sapiens 16-23 26924291-12 2016 Upregulation of miR-34b also induced apoptosis and increased the sensitivity of the cells to the anticancer drugs, whereas transfection with miR-34b-AMO, an inhibitor of miR-34b, reversed the anti-proliferation effect of sirolimus. Sirolimus 221-230 microRNA 34b Homo sapiens 141-148 26924291-12 2016 Upregulation of miR-34b also induced apoptosis and increased the sensitivity of the cells to the anticancer drugs, whereas transfection with miR-34b-AMO, an inhibitor of miR-34b, reversed the anti-proliferation effect of sirolimus. Sirolimus 221-230 microRNA 34b Homo sapiens 141-148 26924291-15 2016 CONCLUSION: Sirolimus increases the sensitivity of human OS cells to anticancer drugs in vitro by up-regulating miR-34b interacting with PAK1 and ABCB1. Sirolimus 12-21 microRNA 34b Homo sapiens 112-119 25190019-6 2014 In the overall analysis, a significant association between pri-miR-34b/c rs4938723 polymorphism and increased cancer susceptibility was found in heterozygous model (TC vs. TT: OR = 1.148, 95%CI 1.034-1.275, P = 0.010) and dominant model (CC + TC vs. TT: OR =1.166, 95%CI 1.028-1.322, P = 0.017). Technetium 165-167 microRNA 34b Homo sapiens 63-70 26861642-5 2016 miR-34b expression and methylation of its promoter were not associated with most clinical parameters assessed; however, miR-34b levels in prednisone-sensitive ALL were significantly different from those in insensitive ALL. Prednisone 138-148 microRNA 34b Homo sapiens 120-127 26861642-7 2016 Furthermore, treatment with the demethylating agent 5-aza-2-deoxycytidine significantly enhanced miR-34b expression levels and decreased the methylation status of its promoter in HL-60 and K562 cells. Decitabine 52-73 microRNA 34b Homo sapiens 97-104 26524015-6 2015 The promoter regions of CpG island in HL-60 and K562 cell lines were methylated, while the bone marrow cells were not methylated in 10 cases of non hematologic diseases children.Through miR-34b expression levels of HL-60 and K562 cell lines significantly increased by decitabine treatment (P < 0.05), and the methylation of leukemia cell line promoter region CpG island was found before and after decitabine treatment, but after administration of decitabine the methylation significantly decreased, suggesting that decitabine has an inhibitory effect on methylation of promoter region CpG island. Decitabine 268-278 microRNA 34b Homo sapiens 186-193 26524015-6 2015 The promoter regions of CpG island in HL-60 and K562 cell lines were methylated, while the bone marrow cells were not methylated in 10 cases of non hematologic diseases children.Through miR-34b expression levels of HL-60 and K562 cell lines significantly increased by decitabine treatment (P < 0.05), and the methylation of leukemia cell line promoter region CpG island was found before and after decitabine treatment, but after administration of decitabine the methylation significantly decreased, suggesting that decitabine has an inhibitory effect on methylation of promoter region CpG island. Decitabine 400-410 microRNA 34b Homo sapiens 186-193 26524015-6 2015 The promoter regions of CpG island in HL-60 and K562 cell lines were methylated, while the bone marrow cells were not methylated in 10 cases of non hematologic diseases children.Through miR-34b expression levels of HL-60 and K562 cell lines significantly increased by decitabine treatment (P < 0.05), and the methylation of leukemia cell line promoter region CpG island was found before and after decitabine treatment, but after administration of decitabine the methylation significantly decreased, suggesting that decitabine has an inhibitory effect on methylation of promoter region CpG island. Decitabine 400-410 microRNA 34b Homo sapiens 186-193 26524015-6 2015 The promoter regions of CpG island in HL-60 and K562 cell lines were methylated, while the bone marrow cells were not methylated in 10 cases of non hematologic diseases children.Through miR-34b expression levels of HL-60 and K562 cell lines significantly increased by decitabine treatment (P < 0.05), and the methylation of leukemia cell line promoter region CpG island was found before and after decitabine treatment, but after administration of decitabine the methylation significantly decreased, suggesting that decitabine has an inhibitory effect on methylation of promoter region CpG island. Decitabine 400-410 microRNA 34b Homo sapiens 186-193 25582471-4 2014 HL-60 and K562 were treated with methyltransferase inhibitor (5-aza-2-dC) for further detection of its methylation status and expression of miR-34b. 5-aza-2-dc 62-72 microRNA 34b Homo sapiens 140-147 25582471-11 2014 After leukemia cell lines HL-60 and K562 were treated with 5-aza-2-dC, the methylated bands became obviously weakened, and the relative expression levels of miR-34b substantially increased 49.5 times and 18.8 times respectively. 5-aza-2-dc 59-69 microRNA 34b Homo sapiens 157-164 24643702-11 2014 E(2) + P4 promoted the expression of let-7a and miR-34b and reduced the expression of Bcl-2 in ovarian cancer cells. e(2) + p4 0-9 microRNA 34b Homo sapiens 48-55 24643702-12 2014 When the expression of let-7a or/and miR-34b was inhibited using miRNA inhibitors, E(2) + P4 treatment did not change the protein level of Bcl-2. e(2) + p4 83-92 microRNA 34b Homo sapiens 37-44 24643702-13 2014 CONCLUSION: E(2) + P4 significantly inhibited the cell survival, promoted the cell apoptosis, induced the expression of let-7a and miR-34b, and reduced the expression of Bcl-2 in ovarian cancer cells. e(2) + p4 12-21 microRNA 34b Homo sapiens 131-138 25190019-6 2014 In the overall analysis, a significant association between pri-miR-34b/c rs4938723 polymorphism and increased cancer susceptibility was found in heterozygous model (TC vs. TT: OR = 1.148, 95%CI 1.034-1.275, P = 0.010) and dominant model (CC + TC vs. TT: OR =1.166, 95%CI 1.028-1.322, P = 0.017). Technetium 243-245 microRNA 34b Homo sapiens 63-70 25190019-7 2014 In subgroup analysis of ethnicity, pri-miR-34b/c rs4938723 polymorphism was significantly associated with an increased cancer susceptibility for Asian population in heterozygous model (TC vs. TT: OR = 1.169, 95%CI 1.031-1.326, P = 0.015) and dominant model (CC + TC vs. TT: OR = 1.185, 95%CI 1.017-1.382, P = 0.030), whereas no significant association for Caucasian population was observed in any genetic models. Technetium 185-187 microRNA 34b Homo sapiens 39-46 24892887-0 2014 Increased striatal adenosine A2A receptor levels is an early event in Parkinson"s disease-related pathology and it is potentially regulated by miR-34b. Adenosine 19-28 microRNA 34b Homo sapiens 143-150 24686393-9 2014 Finally, 5-azacytidine and trichostatin A exposure synergistically increased the expression of miR-34b/c in CLL cells, and transfection of miR-34b or miR-34c into HG3 CLL cells significantly increased apoptosis. Azacitidine 9-22 microRNA 34b Homo sapiens 95-102 24945256-7 2014 In addition, the CC genotype of pri-miR-34b/c rs4938723 was associated with a significant decreased risk of ESCC (CC VS. TT/TC: p = 0.007, OR = 0.82, 95% CI = 0.71-0.95) in Chinese population. Technetium 124-126 microRNA 34b Homo sapiens 36-43 24686393-9 2014 Finally, 5-azacytidine and trichostatin A exposure synergistically increased the expression of miR-34b/c in CLL cells, and transfection of miR-34b or miR-34c into HG3 CLL cells significantly increased apoptosis. trichostatin A 27-41 microRNA 34b Homo sapiens 95-102 24071644-7 2013 Through miR-34b/c-driven c-Myc regulation, USP2a increases intracellular GSH content, thus interfering with the oxidative cascade triggered by chemotherapeutic agents. Glutathione 73-76 microRNA 34b Homo sapiens 8-15 25227823-4 2014 We found that the miR-34b/c rs4938723 polymorphism was significantly associated with increased risk of cancers in the heterozygous model (TC versus TT, OR=1.09, 95% CI=1.01-1.18, P=0.02). Technetium 138-140 microRNA 34b Homo sapiens 18-25 24503183-7 2014 Twenty-seven normal tissues adjacent to tumour were used to evaluate the association between the expression level of miR-34b/c and the polymorphism, which revealed higher expression levels of miR-34b/c in normal renal tissues with TT+TC genotypes than in those with CC genotypes (P < 0.01). tt+tc 231-236 microRNA 34b Homo sapiens 117-124 24503183-7 2014 Twenty-seven normal tissues adjacent to tumour were used to evaluate the association between the expression level of miR-34b/c and the polymorphism, which revealed higher expression levels of miR-34b/c in normal renal tissues with TT+TC genotypes than in those with CC genotypes (P < 0.01). tt+tc 231-236 microRNA 34b Homo sapiens 192-199 23632240-5 2013 RESULTS: We found that the miR-34b/c TC+CC frequency was significantly higher in HCC patients than in controls (adjusted odds ratio [AOR]: 1.580; 95% confidence interval [CI]: 1.029-2.426). Technetium 37-39 microRNA 34b Homo sapiens 27-34 23632240-6 2013 The miR-34b/c CC-TP53 Arg/Arg combination significantly increased the risk of HCC (AOR: 13.644; 95% CI: 1.451-128.301). Arginine 22-25 microRNA 34b Homo sapiens 4-11 23632240-8 2013 CONCLUSIONS: Our findings suggest that loss of the T allele in miR-34b/c T>C, and the miR-34b/c CC-TP53 Arg/Arg combination increases the risk of HCC in the Korean population. Arginine 107-110 microRNA 34b Homo sapiens 89-96 23632240-8 2013 CONCLUSIONS: Our findings suggest that loss of the T allele in miR-34b/c T>C, and the miR-34b/c CC-TP53 Arg/Arg combination increases the risk of HCC in the Korean population. Arginine 111-114 microRNA 34b Homo sapiens 89-96 23504554-5 2013 The gene-gene interaction of miR-34b/c rs4938723 and TP-53 Arg72-Pro showed that the combined genotypes of rs4938723CT/CC and TP-53CG/CC increased the risk of NPC (rs4938723CT/CC + TP-53CG/CC vs. rs4938723 TT+TP-53 CG/CC: OR=1.58, 95 % CI 1.04-2.42, p=0.03). neotetrazolium 53-55 microRNA 34b Homo sapiens 29-36 23305226-3 2013 As a hypovascular tumor with a potential endoplasmic reticulum stress microenvironment, miR-34b was silenced after ER stress inducer thapsigargin (Tg) treatment and negatively regulated by ER stress chaperone glucose regulated protein 78 (GRP78) in pancreatic cancer cells. Thapsigargin 133-145 microRNA 34b Homo sapiens 88-95 23305226-3 2013 As a hypovascular tumor with a potential endoplasmic reticulum stress microenvironment, miR-34b was silenced after ER stress inducer thapsigargin (Tg) treatment and negatively regulated by ER stress chaperone glucose regulated protein 78 (GRP78) in pancreatic cancer cells. Thapsigargin 147-149 microRNA 34b Homo sapiens 88-95 23504554-5 2013 The gene-gene interaction of miR-34b/c rs4938723 and TP-53 Arg72-Pro showed that the combined genotypes of rs4938723CT/CC and TP-53CG/CC increased the risk of NPC (rs4938723CT/CC + TP-53CG/CC vs. rs4938723 TT+TP-53 CG/CC: OR=1.58, 95 % CI 1.04-2.42, p=0.03). cysteinylglycine 131-133 microRNA 34b Homo sapiens 29-36 23183747-3 2013 A potentially functional polymorphism (i.e., rs4938723T/C) in the promoter region of pri-miR-34b/c was predicted to influence the GATA-X binding sites. gata 130-134 microRNA 34b Homo sapiens 89-96 22310291-4 2013 The CpG islands of miR-18b, miR-132, miR-34b/c, miR-148a, miR-450a and miR-542-3p showed methylation patterns congruent with their expression modulations in response to AZA. Decitabine 169-172 microRNA 34b Homo sapiens 37-44 21976676-4 2011 5-Aza-2"-deoxycytidine led to MIR34B/C promoter demethylation and MIR34B reexpression. Decitabine 0-22 microRNA 34b Homo sapiens 30-36 22844323-7 2012 Moreover, a significant gene interaction of the carriers with the combined genotypes of miR-34b/c rs4938723CC and TP53 Arg72Pro CG/CC/GG had a decreased risk of IA, compared with those carrying miR-34b/c rs4938723CT/TT+TP53 Arg72Pro GG/CG/CC combined genotypes. cysteinylglycine 128-130 microRNA 34b Homo sapiens 88-95 22844323-7 2012 Moreover, a significant gene interaction of the carriers with the combined genotypes of miR-34b/c rs4938723CC and TP53 Arg72Pro CG/CC/GG had a decreased risk of IA, compared with those carrying miR-34b/c rs4938723CT/TT+TP53 Arg72Pro GG/CG/CC combined genotypes. cysteinylglycine 128-130 microRNA 34b Homo sapiens 194-201 23155254-6 2012 gammaH2AX foci assay showed that DNA double-strand break repair was delayed in miR-34b/c transfectants. gammah2ax 0-9 microRNA 34b Homo sapiens 79-86 21976676-4 2011 5-Aza-2"-deoxycytidine led to MIR34B/C promoter demethylation and MIR34B reexpression. Decitabine 0-22 microRNA 34b Homo sapiens 66-72 21421997-7 2011 We found that miR-34b is significantly elevated in response to mHTT-Exon-1, and its blockade alters the toxicity of mHTT-Exon-1 in vitro. mhtt-exon-1 63-74 microRNA 34b Homo sapiens 14-21 22082000-6 2011 In HEL cells, homozygous miR-34b/c methylation was associated with miR silencing, and 5-aza-2"-deoxycytidine treatment led to re-expression of both miR-34b and miR-34c, consistent with that both miRs are under the regulation of the same promoter CpG island. Decitabine 86-108 microRNA 34b Homo sapiens 148-155 21558425-6 2011 Depletion of miR-34b or miR-34c in differentiated SH-SY5Y dopaminergic neuronal cells resulted in a moderate reduction in cell viability that was accompanied by altered mitochondrial function and dynamics, oxidative stress and reduction in total cellular adenosin triphosphate content. adenosin triphosphate 255-276 microRNA 34b Homo sapiens 13-20 20309940-5 2011 We observed that the variant genotypes of miR-34b/c rs4938723 were associated with significantly increased HCC risks compared with the wild-type TT genotype (adjusted OR = 1.37, 95% CI =1.06-1.78 for TC; OR = 1.53, 95% CI = 1.02-2.31 for CC and OR = 1.40, 95% CI = 1.10-1.80 for TC/CC). Technetium 200-202 microRNA 34b Homo sapiens 42-49 22113133-5 2011 Our in vivo Tet-On system orthotopic model revealed the tumor-suppressive ability of miR-34b. tetramethylenedisulfotetramine 12-15 microRNA 34b Homo sapiens 85-92 22113133-9 2011 Tet-On induction of miR-34b can cause inhibition of tumor growth and cell proliferation. tetramethylenedisulfotetramine 0-3 microRNA 34b Homo sapiens 20-27 22113133-12 2011 The xenoestrogens diethylstilbestrol and zeranol also showed similar estrogenic effects by inhibiting miR-34b expression and by restoring the protein levels of the miR-34b targets cyclin D1 and JAG1 in MCF-7 cells. Diethylstilbestrol 18-36 microRNA 34b Homo sapiens 102-109 22113133-12 2011 The xenoestrogens diethylstilbestrol and zeranol also showed similar estrogenic effects by inhibiting miR-34b expression and by restoring the protein levels of the miR-34b targets cyclin D1 and JAG1 in MCF-7 cells. Diethylstilbestrol 18-36 microRNA 34b Homo sapiens 164-171 22113133-12 2011 The xenoestrogens diethylstilbestrol and zeranol also showed similar estrogenic effects by inhibiting miR-34b expression and by restoring the protein levels of the miR-34b targets cyclin D1 and JAG1 in MCF-7 cells. Zeranol 41-48 microRNA 34b Homo sapiens 102-109 22113133-12 2011 The xenoestrogens diethylstilbestrol and zeranol also showed similar estrogenic effects by inhibiting miR-34b expression and by restoring the protein levels of the miR-34b targets cyclin D1 and JAG1 in MCF-7 cells. Zeranol 41-48 microRNA 34b Homo sapiens 164-171 22870149-5 2011 The colon cancer cell line study showed an association of the lower expression of miR-124a and miR-34b/c with the methylation of these genes and induction of the expression of these genes with the treatment by 5-aza-2"-deoxycytidine. Decitabine 210-232 microRNA 34b Homo sapiens 95-102 20309940-5 2011 We observed that the variant genotypes of miR-34b/c rs4938723 were associated with significantly increased HCC risks compared with the wild-type TT genotype (adjusted OR = 1.37, 95% CI =1.06-1.78 for TC; OR = 1.53, 95% CI = 1.02-2.31 for CC and OR = 1.40, 95% CI = 1.10-1.80 for TC/CC). Technetium 279-281 microRNA 34b Homo sapiens 42-49 17823410-8 2007 Furthermore, as expected from p53 binding to the mir-34b/c promoter, doxorubicin treatment of wild-type, but not p53-deficient, cells resulted in an increase of mir-34b/mir-34c expression. Doxorubicin 69-80 microRNA 34b Homo sapiens 49-56 17823410-8 2007 Furthermore, as expected from p53 binding to the mir-34b/c promoter, doxorubicin treatment of wild-type, but not p53-deficient, cells resulted in an increase of mir-34b/mir-34c expression. Doxorubicin 69-80 microRNA 34b Homo sapiens 161-168