PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 33262626-11 2020 In the presence of high glucose, the expression levels of lncRNA MIR503HG and miR-503 were up-regulated in HK-2 cells cultured in high glucose. Glucose 24-31 microRNA 503 Homo sapiens 78-85 34144025-5 2021 Triclosan significantly increased the expressions of the six miRNAs, namely miR-15a, miR-107, miR-195, miR-424, miR-497 and miR-503, leading to the downregulation of FASN. Triclosan 0-9 microRNA 503 Homo sapiens 124-131 34349560-0 2021 Long Non-Coding RNA BLACAT1 Induces Tamoxifen Resistance in Human Breast Cancer by Regulating miR-503/Bcl-2 Axis (Retraction). Tamoxifen 36-45 microRNA 503 Homo sapiens 94-101 35013925-2 2022 Here, we explored the activity and mechanism of MIR503 host gene (MIR503HG) in high glucose (HG)-evoked cytotoxicity in HK-2 cells. Glucose 84-91 microRNA 503 Homo sapiens 48-54 35452193-8 2022 METTL3 overexpression evokes N6-methyladenosine (m6 A)-dependent miR-503 biogenesis in endothelial cells. N-methyladenosine 29-47 microRNA 503 Homo sapiens 65-72 33262626-11 2020 In the presence of high glucose, the expression levels of lncRNA MIR503HG and miR-503 were up-regulated in HK-2 cells cultured in high glucose. Glucose 135-142 microRNA 503 Homo sapiens 78-85 31989001-0 2020 miR-503/Apelin-12 mediates high glucose-induced microvascular endothelial cells injury via JNK and p38MAPK signaling pathway. Glucose 32-39 microRNA 503 Homo sapiens 0-7 32210618-0 2020 Long Non-coding RNA BLACAT1 Induces Tamoxifen Resistance in Human Breast Cancer by Regulating miR-503/Bcl-2 Axis. Tamoxifen 36-45 microRNA 503 Homo sapiens 94-101 31894362-1 2020 The chemotherapeutic drug epirubicin increases the exosomal export of miR-503 in endothelial cells. Epirubicin 26-36 microRNA 503 Homo sapiens 70-77 31894362-2 2020 To understand the mechanisms behind this process, we transfected endothelial cells with miR-503 carrying a biotin tag. Biotin 107-113 microRNA 503 Homo sapiens 88-95 31894362-5 2020 Using knock-down systems combined with pull-down analysis, we determined that epirubicin mediates the export of miR-503 by disrupting the interaction between hnRNPA2B1 and miR-503. Epirubicin 78-88 microRNA 503 Homo sapiens 112-119 31894362-5 2020 Using knock-down systems combined with pull-down analysis, we determined that epirubicin mediates the export of miR-503 by disrupting the interaction between hnRNPA2B1 and miR-503. Epirubicin 78-88 microRNA 503 Homo sapiens 172-179 31822509-3 2020 We identified enrichment of histone 3 dimethylation at Arg-8 (H3(Me2)R8) in the promoter regions of miR33b, miR96, and miR503. Arginine 55-58 microRNA 503 Homo sapiens 119-125 31989001-3 2020 Methods: ELISA and qPCR were applied to assess the expression of miR-503 and Apelin-12 in high glucose (HG)-treated microvascular endothelial cells (HMEC-1). Glucose 95-102 microRNA 503 Homo sapiens 65-72 29327155-4 2018 In this study, we explored the role of miR-503 in cisplatin-resistant ovarian cancer. Cisplatin 50-59 microRNA 503 Homo sapiens 39-46 29872500-5 2018 Here we show that resveratrol controls breast cancer cell proliferation by inducing tumor-suppressive miRNAs (miR-34a, miR-424, and miR-503) via the p53 pathway and then by suppressing heterogeneous nuclear ribonucleoprotein A1 (HNRNPA1), which is associated with tumorigenesis and tumor progression. Resveratrol 18-29 microRNA 503 Homo sapiens 132-139 29872500-6 2018 Notably, HNRNPA1 was directly regulated by miR-424 and miR-503, the expression of which were mediated by resveratrol. Resveratrol 105-116 microRNA 503 Homo sapiens 55-62 31035988-6 2019 The level of miR-503 was related to the patients" fasting blood glucose, Cholesterol level, NIHSS score and acute-phase modified Rankin Scale (mRS) (r = 0.49, p = 0.001, r = 0.5, p = 0.009, r = 0.45, p = 0.009, r = 0.48, p = 0.003, CI = 95%). Glucose 64-71 microRNA 503 Homo sapiens 13-20 31035988-6 2019 The level of miR-503 was related to the patients" fasting blood glucose, Cholesterol level, NIHSS score and acute-phase modified Rankin Scale (mRS) (r = 0.49, p = 0.001, r = 0.5, p = 0.009, r = 0.45, p = 0.009, r = 0.48, p = 0.003, CI = 95%). Cholesterol 73-84 microRNA 503 Homo sapiens 13-20 29917206-11 2018 miR-503 was predicted to target IGF-1R mRNA, and miR-503 expression in HUVECs in high glucose was higher than that in normal glucose. Glucose 86-93 microRNA 503 Homo sapiens 49-56 29917206-11 2018 miR-503 was predicted to target IGF-1R mRNA, and miR-503 expression in HUVECs in high glucose was higher than that in normal glucose. Glucose 125-132 microRNA 503 Homo sapiens 49-56 29917206-15 2018 CONCLUSIONS: The present study demonstrates that miR-503 expression in HUVECs is elevated in high glucose condition. Glucose 98-105 microRNA 503 Homo sapiens 49-56 29327155-9 2018 RESULTS: MiR-503 expression was significantly downregulated in cisplatin-resistant ovarian cancer cell line SKOV3/DDP compared with parental SKOV3. Cisplatin 63-72 microRNA 503 Homo sapiens 9-16 29327155-10 2018 Over-expression and knock-down of miR-503 partially regulated apoptotic activity and changed the cisplatin resistance of ovarian cancer cells. Cisplatin 97-106 microRNA 503 Homo sapiens 34-41 29327155-11 2018 In exploring the underlying mechanisms of miR-503 in ovarian cancer cells" resistance to cisplatin, we found that miR-503 can directly target PI3K p85 and participates in the regulation of the PI3K/Akt signaling pathway. Cisplatin 89-98 microRNA 503 Homo sapiens 42-49 29327155-11 2018 In exploring the underlying mechanisms of miR-503 in ovarian cancer cells" resistance to cisplatin, we found that miR-503 can directly target PI3K p85 and participates in the regulation of the PI3K/Akt signaling pathway. Cisplatin 89-98 microRNA 503 Homo sapiens 114-121 29327155-12 2018 In vivo, miR-503 agomirs combined with cisplatin treatment significantly reduced the growth of tumors compared with cisplatin alone. Cisplatin 116-125 microRNA 503 Homo sapiens 9-16 29327155-13 2018 CONCLUSIONS: Our data suggest that miR-503 might be a sensitizer to cisplatin treatment in ovarian cancer by targeting PI3K p85, thus giving a new insight into developing therapeutic strategies to overcome cisplatin resistance in ovarian cancer. Cisplatin 68-77 microRNA 503 Homo sapiens 35-42 29327155-13 2018 CONCLUSIONS: Our data suggest that miR-503 might be a sensitizer to cisplatin treatment in ovarian cancer by targeting PI3K p85, thus giving a new insight into developing therapeutic strategies to overcome cisplatin resistance in ovarian cancer. Cisplatin 206-215 microRNA 503 Homo sapiens 35-42 28912531-7 2017 Furthermore, miR-503 inhibitor augments the growth inhibitory effect of temozolomide in glioblastoma cells. Temozolomide 72-84 microRNA 503 Homo sapiens 13-20 29285014-7 2017 We found that miR-503 was markedly upregulated in placenta tissue from GDM patients, as elevated in peripheral blood specimens, and the high level was positively correlated to blood glucose concentration. Glucose 182-189 microRNA 503 Homo sapiens 14-21 28900284-0 2017 MiR-503 modulates epithelial-mesenchymal transition in silica-induced pulmonary fibrosis by targeting PI3K p85 and is sponged by lncRNA MALAT1. Silicon Dioxide 55-61 microRNA 503 Homo sapiens 0-7 28900284-5 2017 In addition, overexpressed miR-503 inhibited silica-induced pulmonary fibrosis by attenuating the severity and the distribution of lesions in vivo and limiting the process of epithelial-mesenchymal transition (EMT) in vitro. Silicon Dioxide 45-51 microRNA 503 Homo sapiens 27-34 28900284-8 2017 Taken together, our data suggested that MALAT1-miR-503-PI3K/Akt/mTOR/Snail pathway plays critical roles in silica-induced pulmonary fibrosis. Silicon Dioxide 107-113 microRNA 503 Homo sapiens 47-54 28690214-0 2017 [MiR-503 sensitizes human hepatocellular carcinoma cells to cisplatin by targeting bcl-2]. Cisplatin 60-69 microRNA 503 Homo sapiens 1-8 28880936-8 2017 The expression of miR-503 was positively correlated with %FVC, %FEV1, and %DLco as well as IL-6, -8, PGE2, HGF, KGF, and VEGF in the absence or presence of IL-1ss/TNF-alpha. Dinoprostone 101-105 microRNA 503 Homo sapiens 18-25 28880936-14 2017 Endogenous miR-503 was differently regulated by exogenous stimulants associated with COPD pathogenesis, including IL-1ss/TNF-alpha, TGF-ss1 and PGE2. Dinoprostone 144-148 microRNA 503 Homo sapiens 11-18 28690214-6 2017 : Conclusion: MiR-503 may enhance the sensitivity of BEL-7402 cells to cisplatin and inhibit the cell proliferation by targeting bcl-2. Cisplatin 72-81 microRNA 503 Homo sapiens 15-22 27764787-8 2016 Interestingly, the most upregulated transcript (i.e., CXCL10/IP-10) was a validated miR-503 target and CXCL10/IP-10 neutralization significantly reverted the anti-proliferative action of PDGFR-alpha, and PDGFR-alpha inhibition by Dasatinb totally reverted the CXCL10/IP10 induction, further supporting a functional interplay of these factors. dasatinb 230-238 microRNA 503 Homo sapiens 84-91 27840964-0 2017 miR-503 inhibits proliferation making human hepatocellular carcinoma cells susceptible to 5-fluorouracil by targeting EIF4E. Fluorouracil 90-104 microRNA 503 Homo sapiens 0-7 27840964-5 2017 We used MTT to analyze cell proliferation activity and noted that there was a considerable decrease of miR-503 in HCC tissues and cell lines when measured against the controls. monooxyethylene trimethylolpropane tristearate 8-11 microRNA 503 Homo sapiens 103-110 28599480-11 2017 It was found that miR-503 mimics could sensitize the cells to treatment with ADM, TAM and TAX. Doxorubicin 77-80 microRNA 503 Homo sapiens 18-25 28599480-11 2017 It was found that miR-503 mimics could sensitize the cells to treatment with ADM, TAM and TAX. Tamoxifen 82-85 microRNA 503 Homo sapiens 18-25 24486548-5 2014 A statistically significant inverse association was found between miR-503 methylation status and expression of the miR-503 in tumor tissues (P<0.001), and expression of miR-503 was restored by the demethylating agent 5-aza-2"-deoxycytidine, suggesting that methylation was associated with the transcriptional silencing. Decitabine 220-242 microRNA 503 Homo sapiens 66-73 25269574-2 2014 In order to investigate the effects and mechanisms of microRNA-503 (miR-503) in the reversal of Adriamycin (ADM) resistance in the drug-resistant HepG2/ADM hepatocellular cancer cell line, an ADM-resistant HepG2/ADM cell line was established using continuous drug exposure. Doxorubicin 96-106 microRNA 503 Homo sapiens 54-66 25269574-2 2014 In order to investigate the effects and mechanisms of microRNA-503 (miR-503) in the reversal of Adriamycin (ADM) resistance in the drug-resistant HepG2/ADM hepatocellular cancer cell line, an ADM-resistant HepG2/ADM cell line was established using continuous drug exposure. Doxorubicin 96-106 microRNA 503 Homo sapiens 68-75 25269574-2 2014 In order to investigate the effects and mechanisms of microRNA-503 (miR-503) in the reversal of Adriamycin (ADM) resistance in the drug-resistant HepG2/ADM hepatocellular cancer cell line, an ADM-resistant HepG2/ADM cell line was established using continuous drug exposure. Doxorubicin 109-112 microRNA 503 Homo sapiens 54-66 25269574-2 2014 In order to investigate the effects and mechanisms of microRNA-503 (miR-503) in the reversal of Adriamycin (ADM) resistance in the drug-resistant HepG2/ADM hepatocellular cancer cell line, an ADM-resistant HepG2/ADM cell line was established using continuous drug exposure. Doxorubicin 109-112 microRNA 503 Homo sapiens 68-75 25269574-5 2014 Furthermore, miR-503 overexpression was found to increase intracellular rhodamine-123 levels and the rate of apoptosis, block the cell cycle at G0/G1-phase and significantly decrease intracellular superoxide dismutase and glutathione levels. Rhodamine 123 72-85 microRNA 503 Homo sapiens 13-20 24486548-1 2014 It is reported that MicroRNA-503 (miR-503) regulates cell apoptosis, and thus modulates the resistance of non-small cell lung cancer cells (NSCLC) to cisplatin. Cisplatin 150-159 microRNA 503 Homo sapiens 20-32 24486548-1 2014 It is reported that MicroRNA-503 (miR-503) regulates cell apoptosis, and thus modulates the resistance of non-small cell lung cancer cells (NSCLC) to cisplatin. Cisplatin 150-159 microRNA 503 Homo sapiens 34-41 24486548-5 2014 A statistically significant inverse association was found between miR-503 methylation status and expression of the miR-503 in tumor tissues (P<0.001), and expression of miR-503 was restored by the demethylating agent 5-aza-2"-deoxycytidine, suggesting that methylation was associated with the transcriptional silencing. Decitabine 220-242 microRNA 503 Homo sapiens 115-122 24486548-5 2014 A statistically significant inverse association was found between miR-503 methylation status and expression of the miR-503 in tumor tissues (P<0.001), and expression of miR-503 was restored by the demethylating agent 5-aza-2"-deoxycytidine, suggesting that methylation was associated with the transcriptional silencing. Decitabine 220-242 microRNA 503 Homo sapiens 115-122 24486548-7 2014 Taken together, our results suggest that miR-503 regulates the resistance of non-small cell lung cancer cells to cisplatin at least in part by targeting FANCA. Cisplatin 113-122 microRNA 503 Homo sapiens 41-48 24931256-0 2014 MiR-503 regulates cisplatin resistance of human gastric cancer cell lines by targeting IGF1R and BCL2. Cisplatin 18-27 microRNA 503 Homo sapiens 0-7 24931256-9 2014 An in vitro drug sensitivity assay showed that overexpression of miR-503 sensitized SGC7901/DDP cells to cisplatin. Cisplatin 105-114 microRNA 503 Homo sapiens 65-72 24931256-2 2014 We investigated the role of miR-503 in the development of cisplatin resistance in human gastric cancer cell lines. Cisplatin 58-67 microRNA 503 Homo sapiens 28-35 24931256-12 2014 CONCLUSION: Our findings suggest that hsa-miR-503 modulates cisplatin resistance of human gastric cancer cells at least in part by targeting IGF1R and BCL2. Cisplatin 60-69 microRNA 503 Homo sapiens 38-49 24931256-8 2014 Additionally, downregulation of miR-503 in the cisplatin (DDP)-resistant gastric cancer cell line SGC7901/DDP was concurrent with the upregulation of insulin-like growth factor-1 receptor (IGF1R) and B-cell lymphoma 2 (BCL2) expression compared with the parental SGC7901 cell line. Cisplatin 47-56 microRNA 503 Homo sapiens 32-39 24398307-3 2014 The aim of this study is to investigate the effects and molecular mechanisms of miR-503 on reversing the cisplatin-resistance in lung cancer DDP-resistant cell line A549/DDP. Cisplatin 105-114 microRNA 503 Homo sapiens 80-87 24398307-4 2014 METHODS: MTS assay was employed to determine the effect of miR-503 on A549/DDP" sensitivity to cisplatin. Cisplatin 95-104 microRNA 503 Homo sapiens 59-66 24398307-0 2014 [The reversing and molecular mechanisms of miR-503 on the drug-resistance to cisplatin in A549/DDP cells]. Cisplatin 77-86 microRNA 503 Homo sapiens 43-50 24398307-7 2014 RESULTS: MiR-503 was able to increase the cisplatin sensitivity of A549/DDP. Cisplatin 42-51 microRNA 503 Homo sapiens 9-16 24398307-9 2014 CONCLUSIONS: MiR-503 was able to reverse the cisplatin resistance of A549/DDP. Cisplatin 45-54 microRNA 503 Homo sapiens 13-20 23856992-0 2013 miR-503 regulates the resistance of non-small cell lung cancer cells to cisplatin by targeting Bcl-2. Cisplatin 72-81 microRNA 503 Homo sapiens 0-7 23856992-3 2013 In this study, we report that miR-503 regulates the resistance of non-small cell lung cancer cells to cisplatin. Cisplatin 102-111 microRNA 503 Homo sapiens 30-37 23856992-4 2013 The expression of miR-503 was decreased in the cisplatin-resistant non-small cell lung cancer cells, A549/CDDP, compared with the parental A549 cells. Cisplatin 47-56 microRNA 503 Homo sapiens 18-25 23856992-4 2013 The expression of miR-503 was decreased in the cisplatin-resistant non-small cell lung cancer cells, A549/CDDP, compared with the parental A549 cells. Cisplatin 106-110 microRNA 503 Homo sapiens 18-25 23856992-5 2013 The overexpression of miR-503 sensitized the A549/CDDP cells to cisplatin, whereas the inhibition of miR-503 in the A549 cells increased resistance to cisplatin. Cisplatin 64-73 microRNA 503 Homo sapiens 22-29 23856992-5 2013 The overexpression of miR-503 sensitized the A549/CDDP cells to cisplatin, whereas the inhibition of miR-503 in the A549 cells increased resistance to cisplatin. Cisplatin 151-160 microRNA 503 Homo sapiens 101-108 23856992-7 2013 The ectopic expression of miR-503 reduced the Bcl-2 protein level and sensitized the A549/CDDP cells to cisplatin-induced apoptosis. Cisplatin 104-113 microRNA 503 Homo sapiens 26-33 23856992-8 2013 Taken together, our results suggest that miR-503 regulates cell apoptosis, at least in part by targeting Bcl-2, and thus modulates the resistance of non-small cell lung cancer cells to cisplatin. Cisplatin 185-194 microRNA 503 Homo sapiens 41-48 22072795-7 2012 Decreasing the levels of cellular polyamines reduced endogenous miR-503 levels and promoted CUGBP1 expression, an effect that was prevented by ectopic miR-503 overexpression. Polyamines 34-44 microRNA 503 Homo sapiens 64-71 22072795-7 2012 Decreasing the levels of cellular polyamines reduced endogenous miR-503 levels and promoted CUGBP1 expression, an effect that was prevented by ectopic miR-503 overexpression. Polyamines 34-44 microRNA 503 Homo sapiens 151-158 21220732-3 2011 METHODS AND RESULTS: We found that microRNA-503 (miR-503) expression in ECs is upregulated in culture conditions mimicking diabetes mellitus (high D-glucose) and ischemia-associated starvation (low growth factors). Glucose 147-156 microRNA 503 Homo sapiens 35-47 21220732-3 2011 METHODS AND RESULTS: We found that microRNA-503 (miR-503) expression in ECs is upregulated in culture conditions mimicking diabetes mellitus (high D-glucose) and ischemia-associated starvation (low growth factors). Glucose 147-156 microRNA 503 Homo sapiens 49-56 21220732-5 2011 Conversely, blocking miR-503 activity by either adenovirus-mediated transfer of a miR-503 decoy (Ad.decoymiR-503) or by antimiR-503 (antisense oligonucleotide) improved the functional capacities of ECs cultured under high D-glucose/low growth factors. Oligonucleotides 143-158 microRNA 503 Homo sapiens 21-28 21220732-5 2011 Conversely, blocking miR-503 activity by either adenovirus-mediated transfer of a miR-503 decoy (Ad.decoymiR-503) or by antimiR-503 (antisense oligonucleotide) improved the functional capacities of ECs cultured under high D-glucose/low growth factors. Glucose 222-231 microRNA 503 Homo sapiens 21-28 21220732-6 2011 We identified CCNE1 and cdc25A as direct miR-503 targets which are downregulated by high glucose/low growth factors in ECs. Glucose 89-96 microRNA 503 Homo sapiens 41-48