PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 34800749-0 2022 MiR-144-3p targets STC1 to activate PI3K/AKT pathway to induce cell apoptosis and cell cycle arrest in selenium deficiency broilers. Selenium 103-111 microRNA 144 Homo sapiens 0-7 34800749-8 2022 Finally, in order to further understand whether miR-144-3p/STC1 axis is involved in the process, miR-144-3p knockdown and overexpression experiments were carried out, it was found that miR-144-3p inhibitor can reduce the occurrence of cell apoptosis and cell cycle arrest. -144-3p 188-195 microRNA 144 Homo sapiens 48-55 34192826-0 2021 Sevoflurane inhibits neuroblastoma cell proliferation, invasion and induces apoptosis by miR-144-3p/YAP1 axis. Sevoflurane 0-11 microRNA 144 Homo sapiens 89-96 34853730-6 2021 Rap1a mediated inflammation induced by Hcy and serves as a direct target of miR-144. Homocysteine 39-42 microRNA 144 Homo sapiens 76-83 34425095-9 2021 Furthermore, miR-144 overexpression reduces Irg1 expression and the production of itaconate in vitro. itaconic acid 82-91 microRNA 144 Homo sapiens 13-20 34425095-12 2021 miR-144 silencing selectively reduced the activities of both SDH and FH resulting in the accumulation of their related substrates succinate and fumarate. Succinic Acid 130-139 microRNA 144 Homo sapiens 0-7 34425095-12 2021 miR-144 silencing selectively reduced the activities of both SDH and FH resulting in the accumulation of their related substrates succinate and fumarate. Fumarates 144-152 microRNA 144 Homo sapiens 0-7 34425095-14 2021 Combined, these results demonstrate that silencing of miR-144 inhibits the activity of NRF2 through decreased fumarate production in obesity. Fumarates 110-118 microRNA 144 Homo sapiens 54-61 34425095-15 2021 CONCLUSIONS: Herein we unravel a novel mechanism whereby miR-144 inhibits NRF2 activity through the consumption of fumarate by activation of FH. Fumarates 115-123 microRNA 144 Homo sapiens 57-64 34425095-16 2021 Our study demonstrates that hepatic miR-144 triggers a hyperactive FH in the TCA cycle leading to an impaired antioxidant response in obesity. Tricarboxylic Acids 77-80 microRNA 144 Homo sapiens 36-43 34192826-0 2021 Sevoflurane inhibits neuroblastoma cell proliferation, invasion and induces apoptosis by miR-144-3p/YAP1 axis. p-Bis(2-chloroethyl)amino-o-methoxyphenylalanine 97-99 microRNA 144 Homo sapiens 89-96 34192826-11 2021 Furthermore, the dual-luciferase reporter assay confirmed that miR-144-3p targeted YAP1, and overexpressing YAP1 partially weakened the inhibitive effects of miR-144-3p on NB cells. mir-144-3p 158-168 microRNA 144 Homo sapiens 63-70 35245871-7 2022 Therefore, TCS acts on GPER to activate the downstream PKC/MAPK signaling pathway, further up-regulating miR-144 expression and causing abnormal modulation of these nerve-related genes to trigger neurodevelopmental toxicity. Triclosan 11-14 microRNA 144 Homo sapiens 105-112 34542064-14 2022 Rescue studies validated that the miR-144-3p-inhibited glucose metabolism and 5-FU sensitization were through targeting PDK4. Fluorouracil 78-82 microRNA 144 Homo sapiens 34-41 34542064-16 2022 CONCLUSION: In summary, this study reveals critical roles and molecular mechanisms of the HCG11-mediated 5-FU resistance through modulating the miR-144-3p-PDK4-glucose metabolism pathway in CRC. Fluorouracil 105-109 microRNA 144 Homo sapiens 144-151 34542064-16 2022 CONCLUSION: In summary, this study reveals critical roles and molecular mechanisms of the HCG11-mediated 5-FU resistance through modulating the miR-144-3p-PDK4-glucose metabolism pathway in CRC. p-Bis(2-chloroethyl)amino-o-methoxyphenylalanine 152-154 microRNA 144 Homo sapiens 144-151 34311128-9 2021 Furthermore, OIP5-AS1 was identified as a sponge of miR-144-5p, and upregulation of miR-144-5p could significantly reverse overexpression of OIP5-AS1-induced protective effect on the damage of cisplatin to HK-2 cells. Cisplatin 193-202 microRNA 144 Homo sapiens 52-59 34311128-9 2021 Furthermore, OIP5-AS1 was identified as a sponge of miR-144-5p, and upregulation of miR-144-5p could significantly reverse overexpression of OIP5-AS1-induced protective effect on the damage of cisplatin to HK-2 cells. Cisplatin 193-202 microRNA 144 Homo sapiens 84-91 34311128-10 2021 In addition, pyruvate kinase M2 (PKM2) was found to be a direct target of miR-144-5p, and overexpression of PKM2 efficiently reversed the effect of miR-144-5p mimics on the damage in cisplatin-stimulated HK-2 cells. Cisplatin 183-192 microRNA 144 Homo sapiens 74-81 34311128-10 2021 In addition, pyruvate kinase M2 (PKM2) was found to be a direct target of miR-144-5p, and overexpression of PKM2 efficiently reversed the effect of miR-144-5p mimics on the damage in cisplatin-stimulated HK-2 cells. Cisplatin 183-192 microRNA 144 Homo sapiens 148-155 33614632-11 2020 Additionally, LINC01969, which primarily exists in the cytoplasm, boosted LARP1 expression by sponging miR-144-5p and promoted the malignant phenotypes of OC cells. linc01969 14-23 microRNA 144 Homo sapiens 103-110 35204817-6 2022 Circulating miR-199a-5p and miR-144 were associated with hemolytic biomarkers such as LDH, indirect bilirubin, AST, GGT, iron, ferritin, RBC, hemoglobin, and NOm, in addition to association with impaired clinical profile of SLU. Bilirubin 100-109 microRNA 144 Homo sapiens 28-35 35204817-6 2022 Circulating miR-199a-5p and miR-144 were associated with hemolytic biomarkers such as LDH, indirect bilirubin, AST, GGT, iron, ferritin, RBC, hemoglobin, and NOm, in addition to association with impaired clinical profile of SLU. Iron 121-125 microRNA 144 Homo sapiens 28-35 33496921-8 2021 Moreover, the inhibitory effect of circ_0081146 knockdown on the progression of GC cells were reversed by silencing miR-144 or HMGB1 overexpression. circ_0081146 35-47 microRNA 144 Homo sapiens 116-123 33658044-0 2021 Epigenetic silencing of miR-144/451a cluster contributes to HCC progression via paracrine HGF/MIF-mediated TAM remodeling. tam 107-110 microRNA 144 Homo sapiens 24-31 33614632-12 2020 In conclusion, the LINC01969/miR-144-5p/LARP1 axis is a newly identified regulatory signaling pathway involved in OC progression. linc01969 19-28 microRNA 144 Homo sapiens 29-36 32798408-3 2020 MTT assay was used to detect the proliferation and cloning ability of myeloma cells transfected by miR-144. monooxyethylene trimethylolpropane tristearate 0-3 microRNA 144 Homo sapiens 99-106 33116843-13 2020 The expression of miR-144-3p in miR-144-3p-inhibitor group was significantly lower than that in NC group (P<0.01), and that in miR-144-3p-mimics group was significantly higher than that in NC group (p < 0.01). -144-3p 21-28 microRNA 144 Homo sapiens 32-39 33116843-13 2020 The expression of miR-144-3p in miR-144-3p-inhibitor group was significantly lower than that in NC group (P<0.01), and that in miR-144-3p-mimics group was significantly higher than that in NC group (p < 0.01). p-Bis(2-chloroethyl)amino-o-methoxyphenylalanine 26-28 microRNA 144 Homo sapiens 18-25 33116843-13 2020 The expression of miR-144-3p in miR-144-3p-inhibitor group was significantly lower than that in NC group (P<0.01), and that in miR-144-3p-mimics group was significantly higher than that in NC group (p < 0.01). p-Bis(2-chloroethyl)amino-o-methoxyphenylalanine 26-28 microRNA 144 Homo sapiens 32-39 32563146-14 2020 In conclusion, NORAD promoted the progression and DOX resistance of NB through miR-144-3p/HDAC8 axis in vivo and in vitro. Doxorubicin 50-53 microRNA 144 Homo sapiens 79-86 32139705-12 2020 The MTT and cell cycle assay indicated miR-144 suppressed glioma cells proliferation through modulating FGF mediated Akt signaling pathway. monooxyethylene trimethylolpropane tristearate 4-7 microRNA 144 Homo sapiens 39-46 32308422-13 2020 Functionally, FEZF1-AS1 silencing or miR-144 overexpression inhibited cell viability, the glucose and lactate productions and promoted cell apoptosis in Saos-2 and HOS cells. Glucose 90-97 microRNA 144 Homo sapiens 37-44 32308422-13 2020 Functionally, FEZF1-AS1 silencing or miR-144 overexpression inhibited cell viability, the glucose and lactate productions and promoted cell apoptosis in Saos-2 and HOS cells. Lactic Acid 102-109 microRNA 144 Homo sapiens 37-44 32308422-14 2020 Furthermore, miR-144 inhibitor mitigated the inhibitory effects on cell viability, the glucose and lactate productions and the promoted effect on cell apoptosis rate in Saos-2 and HOS cells induced by FEZF1-AS1 depletion. Glucose 87-94 microRNA 144 Homo sapiens 13-20 32308422-14 2020 Furthermore, miR-144 inhibitor mitigated the inhibitory effects on cell viability, the glucose and lactate productions and the promoted effect on cell apoptosis rate in Saos-2 and HOS cells induced by FEZF1-AS1 depletion. Lactic Acid 99-106 microRNA 144 Homo sapiens 13-20 32139705-13 2020 Meanwhile, miR-144 promoted Temozolomide (TMZ) induced apoptosis in glioma cells via increasing ROS production by using FACS. Temozolomide 28-40 microRNA 144 Homo sapiens 11-18 32139705-13 2020 Meanwhile, miR-144 promoted Temozolomide (TMZ) induced apoptosis in glioma cells via increasing ROS production by using FACS. Temozolomide 42-45 microRNA 144 Homo sapiens 11-18 32139705-13 2020 Meanwhile, miR-144 promoted Temozolomide (TMZ) induced apoptosis in glioma cells via increasing ROS production by using FACS. Reactive Oxygen Species 96-99 microRNA 144 Homo sapiens 11-18 31724712-10 2020 miR-144 directly targeted hydroxymethylglutaryl-CoA reductase (hmgcr), cholesterol 7alpha-monooxygenase A1 (cyp7a1), and adenosine triphosphate binding cassette transporter A1 (abca1) in HEK293T cells. Adenosine Triphosphate 121-143 microRNA 144 Homo sapiens 0-7 31945725-8 2020 Knockdown of miR-144-3p elevates the expression of TET2 and total 5hmC levels in BMSCs. Cytosine 66-70 microRNA 144 Homo sapiens 13-20 31724712-0 2020 miR-144 Mediates High Fat-Induced Changes of Cholesterol Metabolism via Direct Regulation of C/EBPalpha in the Liver and Isolated Hepatocytes of Yellow Catfish. Cholesterol 45-56 microRNA 144 Homo sapiens 0-7 31724712-8 2020 The promoter activities of miR-144 were analyzed in HEK293T cells with PA (0.25 mM) or OA (0.25 or 0.5 mM) treatment for 24 h. Luciferase activity assays, electrophoretic mobility shift assay, and Western blotting were conducted in HEK293T cells. Palmitic Acid 71-73 microRNA 144 Homo sapiens 27-34 31724712-10 2020 miR-144 directly targeted hydroxymethylglutaryl-CoA reductase (hmgcr), cholesterol 7alpha-monooxygenase A1 (cyp7a1), and adenosine triphosphate binding cassette transporter A1 (abca1) in HEK293T cells. Cholesterol 71-82 microRNA 144 Homo sapiens 0-7 31724712-11 2020 In the hepatocytes of yellow catfish, miR-144 inversely regulated the expression of hmgcr, cyp7a1, and abca1 (30.3-78.5%, P < 0.05); loss of miR-144 function alleviated PA- or OA-induced cholesterol accumulation (19.5-61.1%, P < 0.05). Palmitic Acid 172-174 microRNA 144 Homo sapiens 38-45 31724712-11 2020 In the hepatocytes of yellow catfish, miR-144 inversely regulated the expression of hmgcr, cyp7a1, and abca1 (30.3-78.5%, P < 0.05); loss of miR-144 function alleviated PA- or OA-induced cholesterol accumulation (19.5-61.1%, P < 0.05). Cholesterol 190-201 microRNA 144 Homo sapiens 38-45 31724712-13 2020 CONCLUSIONS: miR-144 mediated HFD-induced changes in the liver and hepatocytes of yellow catfish, suggesting a possible mechanism for HFD-induced dysfunction in cholesterol metabolism. Cholesterol 161-172 microRNA 144 Homo sapiens 13-20 31907983-3 2020 MiR-144 was identified to be decreased in HG-induced cardiomyocytes and in streptozotocin (STZ)-challenged heart samples. Streptozocin 75-89 microRNA 144 Homo sapiens 0-7 31852219-10 2020 CONCLUSIONS: Our data demonstrate silencing miR-144 has sex-specific effects and that treatment with antisense oligonucleotides to target miR-144 might result in enhancements in reverse cholesterol transport and oxysterol metabolism in patients with cardiovascular disease. Cholesterol 186-197 microRNA 144 Homo sapiens 44-51 31852219-10 2020 CONCLUSIONS: Our data demonstrate silencing miR-144 has sex-specific effects and that treatment with antisense oligonucleotides to target miR-144 might result in enhancements in reverse cholesterol transport and oxysterol metabolism in patients with cardiovascular disease. Cholesterol 186-197 microRNA 144 Homo sapiens 138-145 31852219-10 2020 CONCLUSIONS: Our data demonstrate silencing miR-144 has sex-specific effects and that treatment with antisense oligonucleotides to target miR-144 might result in enhancements in reverse cholesterol transport and oxysterol metabolism in patients with cardiovascular disease. arthrofactin 212-221 microRNA 144 Homo sapiens 138-145 31907983-3 2020 MiR-144 was identified to be decreased in HG-induced cardiomyocytes and in streptozotocin (STZ)-challenged heart samples. Streptozocin 91-94 microRNA 144 Homo sapiens 0-7 31907983-7 2020 Importantly, the systemic neutralization of miR-144 attenuated mitochondrial disorder and ventricular dysfunction following STZ treatment. Streptozocin 124-127 microRNA 144 Homo sapiens 44-51 31894313-0 2020 Metformin alleviates endometrial hyperplasia through the UCA1/miR-144/TGF-beta1/AKT signaling pathway. Metformin 0-9 microRNA 144 Homo sapiens 62-69 32211094-0 2020 MiR-144 affects proliferation and apoptosis of high glucose-induced AC16 cardiomyocytes by regulating CTRP3/JNK signaling. Glucose 52-59 microRNA 144 Homo sapiens 0-7 32211094-13 2020 SP600125 (a JNK inhibitor, 10 mumol/L) attenuated the si-CTRP3-mediated inhibition of proliferation and promotion of apoptosis in AC16 cardiomyocytes transfected with anti-miR-144 and stimulated with HG. pyrazolanthrone 0-8 microRNA 144 Homo sapiens 172-179 31894313-4 2020 Tamoxifen treatment increased the weight of the uterus and the level of UCA1, while decreasing the expression of miR-144. Tamoxifen 0-9 microRNA 144 Homo sapiens 113-120 31894313-6 2020 By contrast, Met reduced cell viability, promoted cell apoptosis, and reduced the expression levels of UCA1, TGF-beta and p-AKT, while upregulating the expression of miR-144 and active Caspase-3 in a dose-dependent manner. Metformin 13-16 microRNA 144 Homo sapiens 166-173 31894313-11 2020 In conclusion, the current study suggested that Met reduces the risk of EH by reducing the expression levels of UCA1, TGF-beta and p-AKT, while increasing the levels of miR-144 and active Caspase-3 in a dose-dependent manner. Metformin 48-51 microRNA 144 Homo sapiens 169-176 31243572-8 2019 In alpha-thalassemia, miR-144 and NRF2 target are associated with glutathione level and anemia severity. Glutathione 66-77 microRNA 144 Homo sapiens 22-29 31803236-5 2019 For further validation, we conducted real-time quantitative reverse transcription (RT)-PCR using samples from DCM patients and a doxorubicin-induced rodent model of cardiomyopathy, revealing that miR-144-3p and miR-451a were down-regulated, and miR-21-5p was up-regulated. Doxorubicin 129-140 microRNA 144 Homo sapiens 196-203 31803236-8 2019 Hub nodes and the number of relationship pairs were then analyzed, and the results showed that two lncRNAs (NONHSAT001691 and NONHSAT006358) targeting miR-144/451 were highly related to DCM. nonhsat006358 126-139 microRNA 144 Homo sapiens 151-158 31243572-10 2019 This study reveals that miR-144 expression was upregulated, whereas NRF2 expression and glutathione levels were decreased in comparison with the untreated condition after miR mimic transfection, while the reduction of miR-144 expression contributed to the increased NRF2 expression and glutathione level compared with the untreated condition after miR inhibitor transfection. Glutathione 286-297 microRNA 144 Homo sapiens 218-225 32999164-0 2020 Ginsenoside Rd Inhibits Glioblastoma Cell Proliferation by Up-Regulating the Expression of miR-144-5p. Ginsenosides 0-11 microRNA 144 Homo sapiens 91-98 32999164-4 2020 Ginsenoside Rd up-regulated the tumor-suppressive miR-144-5p in glioblastoma cells. Ginsenosides 0-11 microRNA 144 Homo sapiens 50-57 32999164-6 2020 After inhibition of miR-144-5p, the effect of Ginsenoside Rd on proliferation inhibition and down-regulation of Toll-like receptor 2 was reduced. Ginsenosides 46-57 microRNA 144 Homo sapiens 20-27 32999164-7 2020 These data demonstrated the ginsenoside Rd/miR-144-5p/Toll-like receptor 2 regulatory nexus that controls the glioblastoma pathogenesis of glioblastoma. Ginsenosides 28-39 microRNA 144 Homo sapiens 43-50 31609763-4 2019 The expression of ANRIL, miR-144 and PBX3 in hepatocellular carcinoma cells was altered simultaneously or respectively by vector/oligonucleotide transfection. Oligonucleotides 129-144 microRNA 144 Homo sapiens 25-32 30546074-9 2019 Moreover, the expression of microRNAs (miR)-144/451, miR-146a, miR-155, and miR-223 was also modulated by TNFalpha and ceramide treatments, in line with cellular observations. Ceramides 119-127 microRNA 144 Homo sapiens 28-47 31243572-11 2019 Moreover, miR-144 overexpression leads to significantly increased sensitivity to oxidative stress at indicated concentrations of hydrogen peroxide (H2O2) and rescued by miR-144 inhibitor. Hydrogen Peroxide 129-146 microRNA 144 Homo sapiens 10-17 31243572-11 2019 Moreover, miR-144 overexpression leads to significantly increased sensitivity to oxidative stress at indicated concentrations of hydrogen peroxide (H2O2) and rescued by miR-144 inhibitor. Hydrogen Peroxide 148-152 microRNA 144 Homo sapiens 10-17 31357838-1 2019 Objective: To investigate the effects and mechanisms of miR-144 on proliferation, apoptosis and cisplatin (DDP) resistance of neuroblastoma cells. Cisplatin 107-110 microRNA 144 Homo sapiens 56-63 31017720-0 2019 miR-144 reverses cisplatin resistance in cervical cancer via targeting LHX2. Cisplatin 17-26 microRNA 144 Homo sapiens 0-7 31357838-0 2019 [Effects of miR-144 on proliferation, apoptosis and cisplatin resistance by targeting MYCN in pediatric neuroblastoma]. Cisplatin 52-61 microRNA 144 Homo sapiens 12-19 31017720-2 2019 We explored the roles and mechanisms of miR-144 in resistance to cisplatin (CDDP) of cervical cancer cells. Cisplatin 65-74 microRNA 144 Homo sapiens 40-47 31017720-2 2019 We explored the roles and mechanisms of miR-144 in resistance to cisplatin (CDDP) of cervical cancer cells. Cisplatin 76-80 microRNA 144 Homo sapiens 40-47 31017720-3 2019 miR-144 and LIM homeobox 2 (LHX2) expression in CDDP-resistant and the parental cells was determined by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot analysis, respectively. Cisplatin 48-52 microRNA 144 Homo sapiens 0-7 31017720-5 2019 Overexpression of miR-144 reduced cell viability, induced cell apoptosis, and inhibited cell migration and invasion after CDDP treatment. Cisplatin 122-126 microRNA 144 Homo sapiens 18-25 31017720-9 2019 Taken together, miR-144 overcomes resistance to CDDP via promoting cell apoptosis and inhibiting invasion through targeting LHX2 in cervical cancer cells. Cisplatin 48-52 microRNA 144 Homo sapiens 16-23 31087038-6 2019 We found that the increase of miR-144 levels, shown to be downregulated in U87 and DBTRG human GB cell lines, as well as in GB tumor samples, promoted the downregulation of mRNA of enzymes involved in bioenergetic pathways, with consequent alterations in cell metabolism, impairment of migratory capacity, and sensitization of DBTRG cells to a chemotherapeutic drug, the dichloroacetate (DCA). Dichloroacetic Acid 371-386 microRNA 144 Homo sapiens 30-37 31087038-6 2019 We found that the increase of miR-144 levels, shown to be downregulated in U87 and DBTRG human GB cell lines, as well as in GB tumor samples, promoted the downregulation of mRNA of enzymes involved in bioenergetic pathways, with consequent alterations in cell metabolism, impairment of migratory capacity, and sensitization of DBTRG cells to a chemotherapeutic drug, the dichloroacetate (DCA). Dichloroacetic Acid 388-391 microRNA 144 Homo sapiens 30-37 31292167-9 2019 In the present study, we focussed on a significantly down-regulated miRNA, miR-144-3p, and investigated its role in high glucose (HG) induced cell proliferation. Glucose 121-128 microRNA 144 Homo sapiens 75-82 31292167-15 2019 In conclusion, we demonstrated that miR-144-3p inhibited high glucose-induced cell proliferation through suppressing FGF16 and MAPK signaling pathway, suggesting a possible role of miR-144-FGF16 in the development of DR. Glucose 62-69 microRNA 144 Homo sapiens 36-43 31292167-15 2019 In conclusion, we demonstrated that miR-144-3p inhibited high glucose-induced cell proliferation through suppressing FGF16 and MAPK signaling pathway, suggesting a possible role of miR-144-FGF16 in the development of DR. Glucose 62-69 microRNA 144 Homo sapiens 181-188 31357838-1 2019 Objective: To investigate the effects and mechanisms of miR-144 on proliferation, apoptosis and cisplatin (DDP) resistance of neuroblastoma cells. Cisplatin 96-105 microRNA 144 Homo sapiens 56-63 31059711-0 2019 Downregulation of miR-144 by triptolide enhanced p85alpha-PTEN complex formation causing S phase arrest of human nasopharyngeal carcinoma cells. triptolide 29-39 microRNA 144 Homo sapiens 18-25 30375717-4 2019 Additionally, low expression of miR-144-5p significantly predicted a poor prognosis in patients with LUSQ by The Cancer Genome Atlas database analyses (overall survival, P = 0.026; disease-free survival, P = 0.023). lusq 101-105 microRNA 144 Homo sapiens 32-39 30412705-9 2019 Treatment of KU812 cells with hemin produced an increase in NRF2 expression and HbF induction that reversed with miR-144 pretreatment. Hemin 30-35 microRNA 144 Homo sapiens 113-120 30542710-3 2018 In the course of the study, we unexpectedly found that miR-144-3p could regulate the cisplatin resistance of lung cancer cells via Nrf2. Cisplatin 85-94 microRNA 144 Homo sapiens 55-62 31566128-0 2019 MiR-144-3p inhibits BMSC proliferation and osteogenic differentiation via targeting FZD4 in steroid-associated osteonecrosis. Steroids 92-99 microRNA 144 Homo sapiens 0-7 31566128-2 2019 OBJECTIVE: The aim of this study was to investigate the effects of miR-144-3p on proliferation and osteogenic differentiation of mesenchymal stem cells (MSCs) from the patients with steroid-associated osteonecrosis (ONFH) and its underlying mechanism. Steroids 182-189 microRNA 144 Homo sapiens 67-74 30542710-0 2018 miR-144-3p regulates the resistance of lung cancer to cisplatin by targeting Nrf2. Cisplatin 54-63 microRNA 144 Homo sapiens 0-7 30542710-6 2018 In addition, we also found that in other cancer cell lines, such as HepG2, miR-144-3p also had the function of regulating cisplatin resistance. Cisplatin 122-131 microRNA 144 Homo sapiens 75-82 29504819-0 2018 Effects of miR-144 on the sensitivity of human anaplastic thyroid carcinoma cells to cisplatin by autophagy regulation. Cisplatin 85-94 microRNA 144 Homo sapiens 11-18 30210684-4 2018 Moreover, miR-144-3p overexpression in PC-3 and DU145 cells by transfection with miR-144-3p mimics significantly inhibited cell proliferation and in vitro by MTT, colony formation assays and suppressed tumor growth in vivo by nude mice model. monooxyethylene trimethylolpropane tristearate 158-161 microRNA 144 Homo sapiens 10-17 30210684-4 2018 Moreover, miR-144-3p overexpression in PC-3 and DU145 cells by transfection with miR-144-3p mimics significantly inhibited cell proliferation and in vitro by MTT, colony formation assays and suppressed tumor growth in vivo by nude mice model. monooxyethylene trimethylolpropane tristearate 158-161 microRNA 144 Homo sapiens 81-88 29260980-0 2018 Baohuoside-I suppresses cell proliferation and migration by up-regulating miR-144 in melanoma. baohuoside I 0-12 microRNA 144 Homo sapiens 74-81 29260980-12 2018 Mechanistically, baohuoside-I up-regulated miR-144 expression levels (3 +- 0.2-fold). baohuoside I 17-29 microRNA 144 Homo sapiens 43-50 29260980-13 2018 Silence of miR-144 reversed the inhibition of baohuoside-I in melanoma. baohuoside I 46-58 microRNA 144 Homo sapiens 11-18 30210911-6 2018 Importantly, miR-144 was identified as the hsa_circ_0020123-associated miRNA through performing RNA in vivo precipitation (RIP) in NSCLC cells using a biotin-labeled hsa_circ_0020123 probe. Biotin 151-157 microRNA 144 Homo sapiens 13-20 30108506-0 2018 Lico A Causes ER Stress and Apoptosis via Up-Regulating miR-144-3p in Human Lung Cancer Cell Line H292. lico a 0-6 microRNA 144 Homo sapiens 56-63 30108506-5 2018 Knockdown of miR-144-3p significantly abrogated the apoptosis and proliferation-inhibiting effects of lico A, and lico A could enhance the proliferation-inhibiting effect and apoptosis induced by miR-144-3p overexpression. licochalcone A 102-108 microRNA 144 Homo sapiens 13-20 30108506-5 2018 Knockdown of miR-144-3p significantly abrogated the apoptosis and proliferation-inhibiting effects of lico A, and lico A could enhance the proliferation-inhibiting effect and apoptosis induced by miR-144-3p overexpression. licochalcone A 102-108 microRNA 144 Homo sapiens 196-203 30108506-5 2018 Knockdown of miR-144-3p significantly abrogated the apoptosis and proliferation-inhibiting effects of lico A, and lico A could enhance the proliferation-inhibiting effect and apoptosis induced by miR-144-3p overexpression. licochalcone A 114-120 microRNA 144 Homo sapiens 196-203 30108506-6 2018 Moreover, overexpression miR-144-3p could induce ER stress by down-regulating Nrf2, and lico A enhanced the Nrf2 down-regulation caused by miR-144-3p overexpression. licochalcone A 88-94 microRNA 144 Homo sapiens 25-32 30108506-6 2018 Moreover, overexpression miR-144-3p could induce ER stress by down-regulating Nrf2, and lico A enhanced the Nrf2 down-regulation caused by miR-144-3p overexpression. licochalcone A 88-94 microRNA 144 Homo sapiens 139-146 30108506-7 2018 Co-transfection experiments showed that lico A potentially increased the dicing of pre-miR-144 so as to increase the mature miR-144-3p level. licochalcone A 40-46 microRNA 144 Homo sapiens 87-94 30108506-7 2018 Co-transfection experiments showed that lico A potentially increased the dicing of pre-miR-144 so as to increase the mature miR-144-3p level. licochalcone A 40-46 microRNA 144 Homo sapiens 124-131 28653602-2 2018 miR-144-3p was downregulated in PC tissues and cells. p-Bis(2-chloroethyl)amino-o-methoxyphenylalanine 8-10 microRNA 144 Homo sapiens 0-7 29504819-1 2018 BACKGROUND: We investigated the influence of miR-144 on the cisplatin-sensitivity of anaplastic thyroid carcinoma (ATC) cells and explored the internal molecular mechanism of miR-144. Cisplatin 60-69 microRNA 144 Homo sapiens 45-52 29504819-9 2018 RESULTS: MiR-144, which was low expressed in ATC cells and tissues, could inhibit autophagy activation induced by cisplatin, enhancing the sensitivity of ATC cells to cisplatin, and promoting cell apoptosis. Cisplatin 114-123 microRNA 144 Homo sapiens 9-16 29504819-9 2018 RESULTS: MiR-144, which was low expressed in ATC cells and tissues, could inhibit autophagy activation induced by cisplatin, enhancing the sensitivity of ATC cells to cisplatin, and promoting cell apoptosis. Cisplatin 167-176 microRNA 144 Homo sapiens 9-16 29504819-11 2018 MiR-144 could improve the sensitivity of ATC cells to cisplatin and inhibit tumor growth by suppressing TGF-alpha both in vitro and in vivo. Cisplatin 54-63 microRNA 144 Homo sapiens 0-7 29504819-12 2018 CONCLUSION: MiR-144 could inhibit autophagy of ATC cells by down-regulating TGF-alpha, enhancing the cisplatin-sensitivity of ATC cells. Cisplatin 101-110 microRNA 144 Homo sapiens 12-19 29632436-13 2018 In addition, the blockage of miR-144-3p forced the anti-tumor effect delivered by X-ray exposure or paclitaxel. Paclitaxel 100-110 microRNA 144 Homo sapiens 29-36 29772548-4 2018 Accumulating studies have revealed that miRNAs such as miR-33, miR-27, miR-144, miR-758 and miR-20 are involved in the post-transcriptional control of ABCA1, ABCG1 and SCARB1 genes regulatory network of the reverse cholesterol transport (RCT). Cholesterol 215-226 microRNA 144 Homo sapiens 71-78 29738455-8 2018 Out of these, three miRNAs (miR-144, miR-142, and miR-96) could putatively recognize the 3&rsquo;UTR of the GR gene and three miRNAs (miR-363, miR-96, miR-142) contained GREs sequences, thereby potentially enabling direct regulation by the GR. 3& 89-94 microRNA 144 Homo sapiens 28-35 29387244-7 2018 The present results indicated that the overexpression of miR-144 may significantly inhibit proliferation and promote apoptosis of MG-63 and U-2 cells compared with scramble control. Magnesium 130-132 microRNA 144 Homo sapiens 57-64 29445078-6 2018 SKOV3/OVCAR3 cells were transfected with miR-144 mimics by Lipofectamine, and the proliferation, migration, and invasion ability of these cells were detected by MTT assay, wound healing assay, and Transwell assays, respectively. Lipofectamine 59-72 microRNA 144 Homo sapiens 41-48 27941431-6 2017 In addition, circulating levels of miR-134, -10a, -195, -133b were significantly lower and miR-144, -142-5p, -155 were higher (P < 0.05) with development of BOS. N-[4-(Aminosulfonyl)phenyl]-2-Mercaptobenzamide 160-163 microRNA 144 Homo sapiens 91-98 29312565-6 2017 Of particular significance, miR-144-5p exhibits a high positive correlation with oxoglutaric acid, isocitrate dehydrogenase (IDH) 1 and 2 that involved in the TCA cycle. Ketoglutaric Acids 81-97 microRNA 144 Homo sapiens 28-35 29312565-6 2017 Of particular significance, miR-144-5p exhibits a high positive correlation with oxoglutaric acid, isocitrate dehydrogenase (IDH) 1 and 2 that involved in the TCA cycle. Trichloroacetic Acid 159-162 microRNA 144 Homo sapiens 28-35 29312565-7 2017 Furthermore,we discovered that miR-144-5p regulates TCA cycle metabolism through IDH1 and IDH2. Trichloroacetic Acid 52-55 microRNA 144 Homo sapiens 31-38 29312565-8 2017 Collectively, we describe for the first time the hepatoprotective effect of geniposide decreased miR-144-5p level, capable of regulating TCA cycle by directly targeting IDH1 and IDH2 and promoting functional consequences in cells. geniposide 76-86 microRNA 144 Homo sapiens 97-104 29312565-8 2017 Collectively, we describe for the first time the hepatoprotective effect of geniposide decreased miR-144-5p level, capable of regulating TCA cycle by directly targeting IDH1 and IDH2 and promoting functional consequences in cells. Trichloroacetic Acid 137-140 microRNA 144 Homo sapiens 97-104 28938628-1 2017 The dysregulation expression of microRNAs (miRNAs) including miR-144, has been widely documented in TBI. Thioacetazone 100-103 microRNA 144 Homo sapiens 61-68 28663050-2 2017 Nuclear factor erythroid 2-related factor 2 (NRF2), a potential target of miR-144, is a central regulator of antioxidant response, and plays an important role in glutathione (GSH) biosynthesis and recycling. Glutathione 162-173 microRNA 144 Homo sapiens 74-81 28663050-2 2017 Nuclear factor erythroid 2-related factor 2 (NRF2), a potential target of miR-144, is a central regulator of antioxidant response, and plays an important role in glutathione (GSH) biosynthesis and recycling. Glutathione 175-178 microRNA 144 Homo sapiens 74-81 28663050-6 2017 GSH and glutathion peroxidase (GPX) activities were detected to reveal the effect of miR-144 on GSH accumulation. Glutathione 96-99 microRNA 144 Homo sapiens 85-92 28663050-8 2017 In oxidative stress conditions, miR-144 increased the intracellular accumulation of ROS, reduced cell viability, reduced the activities of GSH and antioxidant enzymes, GPX1, and decreased the expression of GCLC, GCLM, GR and NRF2. Reactive Oxygen Species 84-87 microRNA 144 Homo sapiens 32-39 28663050-8 2017 In oxidative stress conditions, miR-144 increased the intracellular accumulation of ROS, reduced cell viability, reduced the activities of GSH and antioxidant enzymes, GPX1, and decreased the expression of GCLC, GCLM, GR and NRF2. Glutathione 139-142 microRNA 144 Homo sapiens 32-39 28663050-9 2017 In conclusion, miR-144 modulates oxidative stress tolerance by regulating NRF2 expression and GSH generation, which may contribute to the pathogenesis of AD. Glutathione 94-97 microRNA 144 Homo sapiens 15-22 28938628-5 2017 In vitro, miR-144 knockdown protected neuron against Glu-induced injury, by enhancing cell viability, suppressing LDH release and caspase-3 activity, and reducing cognitive-related proteins levels. Glutamic Acid 53-56 microRNA 144 Homo sapiens 10-17 28938628-12 2017 Taken together, these findings demonstrated that elevated miR-144 promoted cognitive impairments induced by beta-amyloid accumulation post-TBI through suppressing of ADAM10 expression. Thioacetazone 139-142 microRNA 144 Homo sapiens 58-65 28225172-0 2017 MiR-144 affects fatty acid composition by regulating ELOVL6 expression in duck hepatocytes. Fatty Acids 16-26 microRNA 144 Homo sapiens 0-7 27297132-4 2016 miR-144 down-regulated the synthesis of PGE2 during pregnancy by directly and indirectly inhibiting COX2 expression and by directly inhibiting the expression of c-fos, a transcriptional activator of COX2 and miR-144. Dinoprostone 40-44 microRNA 144 Homo sapiens 0-7 28383034-6 2017 We identified and validated the transcription factor cAMP-responsive element binding protein (Creb1) and its transcriptional co-activators (Crtc1-3) as targets of miR-17, miR-144, and miR-21. Cyclic AMP 53-57 microRNA 144 Homo sapiens 171-178 26945479-2 2016 miR-33 and miR-144 regulate adenosine triphosphate binding cassette transporter (ABCA1) and other target genes involved in cholesterol efflux, fatty acid oxidation and inflammation. Cholesterol 123-134 microRNA 144 Homo sapiens 11-18 26945479-2 2016 miR-33 and miR-144 regulate adenosine triphosphate binding cassette transporter (ABCA1) and other target genes involved in cholesterol efflux, fatty acid oxidation and inflammation. Fatty Acids 143-153 microRNA 144 Homo sapiens 11-18 27508019-7 2016 Moreover, Enhancement of 5-FU-induced cytotoxicity and apoptosis are resulted from the transfection with miR-144 mimics in Bel-7402/5-FU cells. Fluorouracil 25-29 microRNA 144 Homo sapiens 105-112 27508019-7 2016 Moreover, Enhancement of 5-FU-induced cytotoxicity and apoptosis are resulted from the transfection with miR-144 mimics in Bel-7402/5-FU cells. Fluorouracil 132-136 microRNA 144 Homo sapiens 105-112 28225172-6 2017 When ELOVL6 expression suppressed (miR-144 mimics transfected), the palmitic acid (C16:0) content was significantly increased (P < 0.05); the oleic acid (C18:1, n-9), eicosenoic acid (C20:1, n-9), and eicosatrienoic acid (C20:3) contents were significantly reduced (P < 0.05). Palmitic Acid 68-81 microRNA 144 Homo sapiens 35-42 28225172-6 2017 When ELOVL6 expression suppressed (miR-144 mimics transfected), the palmitic acid (C16:0) content was significantly increased (P < 0.05); the oleic acid (C18:1, n-9), eicosenoic acid (C20:1, n-9), and eicosatrienoic acid (C20:3) contents were significantly reduced (P < 0.05). Palmitic Acid 83-86 microRNA 144 Homo sapiens 35-42 28225172-6 2017 When ELOVL6 expression suppressed (miR-144 mimics transfected), the palmitic acid (C16:0) content was significantly increased (P < 0.05); the oleic acid (C18:1, n-9), eicosenoic acid (C20:1, n-9), and eicosatrienoic acid (C20:3) contents were significantly reduced (P < 0.05). Oleic Acid 145-155 microRNA 144 Homo sapiens 35-42 28225172-8 2017 It indicated that miR-144 could regulate some saturated fatty acids elongated to longer unsaturated fatty acids through controlling ELOVL6 expression. Fatty Acids 46-67 microRNA 144 Homo sapiens 18-25 28225172-8 2017 It indicated that miR-144 could regulate some saturated fatty acids elongated to longer unsaturated fatty acids through controlling ELOVL6 expression. Fatty Acids, Unsaturated 88-111 microRNA 144 Homo sapiens 18-25 28225172-10 2017 Our findings suggest that miR-144 might regulate the percentages of fatty acids in duck hepatocytes through affecting ELOVL6 expression. Fatty Acids 68-79 microRNA 144 Homo sapiens 26-33 28229969-4 2017 Subsequently, overexpression of miR-144 was transfected into HCC cell lines so as to investigate its biological function, including MTT, colony formation, and transwell assays. monooxyethylene trimethylolpropane tristearate 132-135 microRNA 144 Homo sapiens 32-39 26175178-5 2016 The expression of platelet miR-144 and miR-223 significantly correlated with their plasma levels, P2Y12 and IRS-1 expression, blood glucose concentration, and platelet activation rate. Glucose 132-139 microRNA 144 Homo sapiens 27-34 26175178-6 2016 High glucose concentration significantly elevated P-selectin, miR-144 and P2Y12 expression and significantly reduced miR-223 and IRS-1 expression in UT-7 cells. Glucose 5-12 microRNA 144 Homo sapiens 62-69 26175178-7 2016 Overexpression of miR-223 and blocking of miR-144 expression significantly normalized the effects of high glucose concentration in UT-7 cells. Glucose 106-113 microRNA 144 Homo sapiens 42-49 27297132-4 2016 miR-144 down-regulated the synthesis of PGE2 during pregnancy by directly and indirectly inhibiting COX2 expression and by directly inhibiting the expression of c-fos, a transcriptional activator of COX2 and miR-144. Dinoprostone 40-44 microRNA 144 Homo sapiens 208-215 27748283-10 2016 INTERPRETATION & CONCLUSIONS: Our findings showed significant upregulation of miR-144 in serum samples of EC patients indicating its potential as minimally invasive marker. Adenosine Monophosphate 16-19 microRNA 144 Homo sapiens 82-89 27313692-6 2016 Glucose uptake rate and lactate production assays demonstrated that miR-144 expression is decreased and therefore enhances the aerobic metabolism in lung cancer cells. Glucose 0-7 microRNA 144 Homo sapiens 68-75 27313692-6 2016 Glucose uptake rate and lactate production assays demonstrated that miR-144 expression is decreased and therefore enhances the aerobic metabolism in lung cancer cells. Lactic Acid 24-31 microRNA 144 Homo sapiens 68-75 27313692-7 2016 In addition, western blot analysis revealed that miR-144 performs this function by increasing the expression of glucose transporter 1 (GLUT1), leading to an increase in glucose uptake and lactate production. Glucose 112-119 microRNA 144 Homo sapiens 49-56 27313692-7 2016 In addition, western blot analysis revealed that miR-144 performs this function by increasing the expression of glucose transporter 1 (GLUT1), leading to an increase in glucose uptake and lactate production. Lactic Acid 188-195 microRNA 144 Homo sapiens 49-56 26662316-5 2016 As a result, cells overexpressing miR-144 exhibited a metabolic shift, including enhanced glucose uptake and lactate production. Glucose 90-97 microRNA 144 Homo sapiens 34-41 26662316-5 2016 As a result, cells overexpressing miR-144 exhibited a metabolic shift, including enhanced glucose uptake and lactate production. Lactic Acid 109-116 microRNA 144 Homo sapiens 34-41 26662316-6 2016 The altered glucose metabolism induced by miR-144 also leads to a rapid growth of ovarian cancer cells. Glucose 12-19 microRNA 144 Homo sapiens 42-49 25854173-13 2015 MTT and Transwell assays showed that the invasion and metastasis of F5M2 cells was significantly decreased following exogenous overexpression of miR-144. monooxyethylene trimethylolpropane tristearate 0-3 microRNA 144 Homo sapiens 145-152 26566625-0 2015 VEGF-activated miR-144 regulates autophagic survival of prostate cancer cells against Cisplatin. Cisplatin 86-95 microRNA 144 Homo sapiens 15-22 26566625-5 2015 Moreover, microRNA (miR)-144 levels were significantly downregulated in cisplatin-treated PC cells, in a VEGF-dependent manner. Cisplatin 72-81 microRNA 144 Homo sapiens 10-28 26566625-7 2015 In PC patients after cisplatin treatment, low miR-144 levels appeared to predict poor outcome of patients" survival. Cisplatin 21-30 microRNA 144 Homo sapiens 46-53 26566625-8 2015 Together, these data suggest that cisplatin may induce VEGF to suppress miR-144 levels in PC cells, which subsequently upregulates Beclin-1 to increase autophagic cell survival against cisplatin-induced cell death. Cisplatin 34-43 microRNA 144 Homo sapiens 72-79 26566625-9 2015 Upregulation of miR-144 or suppression of cell autophagy may improve the outcome of cisplatin therapy in PC. Cisplatin 84-93 microRNA 144 Homo sapiens 16-23 26595608-10 2015 We find that hsa-miR144 modulates NRF2 activity during ROS stress. Reactive Oxygen Species 55-58 microRNA 144 Homo sapiens 17-23 26250785-9 2015 Over-expression of miR-144-3p inhibited survival capability and increased apoptosis, resulting in enhancement of radiation and temozolomide sensitivity. Temozolomide 127-139 microRNA 144 Homo sapiens 19-26 25979625-8 2015 RESULTS: Analysis of miR-144 in the biopsy specimens demonstrated 4.1 +- 0.8-fold increases in BOS(+) compared with BOS(-) patients, with a significant reduction in TGIF1 (3.6 +- 1.2-fold), a corepressor of Smads. N-[4-(Aminosulfonyl)phenyl]-2-Mercaptobenzamide 95-98 microRNA 144 Homo sapiens 21-28 25979625-8 2015 RESULTS: Analysis of miR-144 in the biopsy specimens demonstrated 4.1 +- 0.8-fold increases in BOS(+) compared with BOS(-) patients, with a significant reduction in TGIF1 (3.6 +- 1.2-fold), a corepressor of Smads. N-[4-(Aminosulfonyl)phenyl]-2-Mercaptobenzamide 116-119 microRNA 144 Homo sapiens 21-28 25979625-11 2015 CONCLUSIONS: miR-144 is a critical regulator of the TGF-beta signaling cascade and is over-expressed in lungs with BOS. N-[4-(Aminosulfonyl)phenyl]-2-Mercaptobenzamide 115-118 microRNA 144 Homo sapiens 13-20 26078353-7 2015 Both bioinformatics and luciferase reporter assays demonstrated that TUG1 influenced BTB permeability via binding to miR-144. btb 85-88 microRNA 144 Homo sapiens 117-124 26078353-10 2015 In conclusion, our results indicate that knockdown of TUG1 increased BTB permeability via binding to miR-144 and then reducing EC tight junction protein expression by targeting HSF2. btb 69-72 microRNA 144 Homo sapiens 101-108 25237911-7 2014 Ectopic expression of miR-144/451a in melanoma cell lines resulted in markedly higher levels of mature miR-451a.1 than miR451a or miR-144; and significantly retarded cell migration and inhibited invasion in a glucose-sensitive manner. Glucose 209-216 microRNA 144 Homo sapiens 22-29 26030000-4 2015 Here, we demonstrate that in SkBr3 breast cancer and HepG2 hepatocarcinoma cells, 17beta-estradiol (E2) and the selective GPER ligand G-1 induce miR144 expression through GPER and the involvement of the PI3K/ERK1/2/Elk1 transduction pathway. Estradiol 82-98 microRNA 144 Homo sapiens 145-151 22842456-0 2012 Myc induced miR-144/451 contributes to the acquired imatinib resistance in chronic myelogenous leukemia cell K562. Imatinib Mesylate 52-60 microRNA 144 Homo sapiens 12-19 24642088-7 2014 Overexpression of miR-144 decreased the expression of IDH2 and the levels of NADPH. NADP 77-82 microRNA 144 Homo sapiens 18-25 24642088-11 2014 Infusion of 7-KC in vivo decreased vascular IDH2 expression and impaired vascular reactivity via miR-144. 7-ketocholesterol 12-16 microRNA 144 Homo sapiens 97-104 24453045-0 2014 Requirement of miR-144 in CsA induced proliferation and invasion of human trophoblast cells by targeting titin. Cyclosporine 26-29 microRNA 144 Homo sapiens 15-22 24453045-2 2014 In this study, with the treatment of CsA (Cyclosporin A), we showed that miR144 expression levels were decreased while titin mRNA expression levels were increased in human trophoblast (HT) cells, and identified titin as a novel direct target of miR-144. Cyclosporine 37-40 microRNA 144 Homo sapiens 73-79 24453045-2 2014 In this study, with the treatment of CsA (Cyclosporin A), we showed that miR144 expression levels were decreased while titin mRNA expression levels were increased in human trophoblast (HT) cells, and identified titin as a novel direct target of miR-144. Cyclosporine 37-40 microRNA 144 Homo sapiens 245-252 24733347-0 2014 An agomir of miR-144-3p accelerates plaque formation through impairing reverse cholesterol transport and promoting pro-inflammatory cytokine production. Cholesterol 79-90 microRNA 144 Homo sapiens 13-20 24733347-4 2014 Moreover, miR-144-3p mimics (agomir) enhanced the expression of inflammatory factors, including IL-1beta, IL-6 and TNF-alpha, in vivo and in vitro, inhibited cholesterol efflux in THP-1 macrophage-derived foam cells, decreased HDL-C circulation and impaired RCT in vivo, resulting in accelerated pathological progression of atherosclerosis in apoE-/- mice. Cholesterol 158-169 microRNA 144 Homo sapiens 10-17 24733347-6 2014 CONCLUSIONS: Our findings clearly indicate that miR-144-3p is essential for the regulation of cholesterol homeostasis and inflammatory reactions, supporting its utility as a potential therapeutic target of atherosclerosis and a promising diagnostic biomarker of AMI. Cholesterol 94-105 microRNA 144 Homo sapiens 48-55 23584289-11 2013 Increases in miR-144 and miR-21 were associated with plasma 8-hydroxydeoxyguanosine 8-OHdG level and were blunted by antioxidant (i.e, DEN). 8-hydroxydeoxyguanosine 8-ohdg 60-90 microRNA 144 Homo sapiens 13-20 23584289-11 2013 Increases in miR-144 and miR-21 were associated with plasma 8-hydroxydeoxyguanosine 8-OHdG level and were blunted by antioxidant (i.e, DEN). Diethylnitrosamine 135-138 microRNA 144 Homo sapiens 13-20 22983984-5 2012 We also investigated changes in sensitivity to the mTOR inhibitor, rapamycin, in inhibitor miR-144-transfected cells. Sirolimus 67-76 microRNA 144 Homo sapiens 91-98 22955854-7 2012 Pre-miR144 treatment and the resultant repression of ZFX in GC cell lines moderately upregulated their susceptibility to 5-fluorouracil chemotherapy. Fluorouracil 121-135 microRNA 144 Homo sapiens 4-10 22842456-3 2012 In this study, we first found that c-myc expression is upregulated in imatinib resistant K562R cells, which in turn enhances the expression of miR-144/451. Imatinib Mesylate 70-78 microRNA 144 Homo sapiens 143-150 22842456-4 2012 Knockdown of c-myc or restoration of miR-144/451 in the K562R cells sensitizes K562R cells to imatinib therapy. Imatinib Mesylate 94-102 microRNA 144 Homo sapiens 37-44 22842456-5 2012 Our study here reveals an regulatory pathway between myc and miR-144/451 and highlights that targeting either myc or miR-144/451 might be valuable for eliminating the imatinib resistant CML cells. Imatinib Mesylate 167-175 microRNA 144 Homo sapiens 61-68 22842456-5 2012 Our study here reveals an regulatory pathway between myc and miR-144/451 and highlights that targeting either myc or miR-144/451 might be valuable for eliminating the imatinib resistant CML cells. Imatinib Mesylate 167-175 microRNA 144 Homo sapiens 117-124 21367459-7 2011 It is concluded that miR-144* might involve in regulation of anti-TB immunity through modification of cytokine production and cell proliferation of T cells. Terbium 66-68 microRNA 144 Homo sapiens 21-28 23226399-5 2012 Here, we show that cigarette smoke and cadmium up-regulate the expression of two miRNAs (miR-101 and miR-144) that are predicted to target CFTR in human bronchial epithelial cells. Cadmium 39-46 microRNA 144 Homo sapiens 101-108 21929751-10 2011 Lastly, DAPT-mediated inhibition of Notch-1 resulted in HCT116 tumor growth arrest and down regulation of Notch-1 via a miR-144 dependent mechanism. dapt 8-12 microRNA 144 Homo sapiens 120-127 20709907-6 2010 We further demonstrate that increased miR-144 is associated with reduced NRF2 levels in HbSS reticulocytes and with decreased glutathione regeneration and attenuated antioxidant capacity in HbSS erythrocytes, thereby providing a possible mechanism for the reduced oxidative stress tolerance and increased anemia severity seen in HbSS patients. Glutathione 126-137 microRNA 144 Homo sapiens 38-45 20709907-6 2010 We further demonstrate that increased miR-144 is associated with reduced NRF2 levels in HbSS reticulocytes and with decreased glutathione regeneration and attenuated antioxidant capacity in HbSS erythrocytes, thereby providing a possible mechanism for the reduced oxidative stress tolerance and increased anemia severity seen in HbSS patients. hbss 88-92 microRNA 144 Homo sapiens 38-45 20708014-8 2010 Furthermore, inhibition of COX-2 activity by either NS-398 or DUP-697 partially offset protective effects of the miR-144/451 cluster. Nitrogen 52-54 microRNA 144 Homo sapiens 113-120