PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28345805-7 2017 Furthermore, the expression level of MEG3 and miR-770 was significantly increased in cancer cells after treated with 5-Aza-dC. Decitabine 117-125 maternally expressed 3 Homo sapiens 37-41 28959364-5 2017 In addition, the cells were treated with decitabine to investigate the correlation between the MEG3 expression and the DNA methylation. Decitabine 41-51 maternally expressed 3 Homo sapiens 95-99 28175963-7 2017 Curcumin led to demethylation in the promoter region of MEG3 and 5-AZA-dC treatment restored MEG3 expression in a dose dependent manner. Decitabine 65-73 maternally expressed 3 Homo sapiens 93-97 28539329-4 2017 Significant downregulation of MEG3 was detected in esophageal cancer cells and ESCC tissues and the expression level of MEG3 was significantly increased in cancer cells after treated with the DNA methyltransferase inhibitor 5-Aza-dC. Decitabine 224-232 maternally expressed 3 Homo sapiens 30-34 28539329-4 2017 Significant downregulation of MEG3 was detected in esophageal cancer cells and ESCC tissues and the expression level of MEG3 was significantly increased in cancer cells after treated with the DNA methyltransferase inhibitor 5-Aza-dC. Decitabine 224-232 maternally expressed 3 Homo sapiens 120-124 26676363-4 2016 Treatment of glioma cells with the DNA methylation inhibitor 5-Aza-2"-deoxycytidine (5-AzadC) decreased aberrant hypermethylation of the MEG3 promoter and prevented the loss of MEG3 expression. Decitabine 61-83 maternally expressed 3 Homo sapiens 137-141 27778235-8 2016 DNA-demethylating agent (5-aza-2-deoxy-cytidine (5-aza-CdR)) treatment significantly increased MEG3 expression level in ESCC cells, and TCGA esophageal cancer dataset also showed that DNA methylation of MEG3 predicted survival. Decitabine 25-47 maternally expressed 3 Homo sapiens 95-99 27778235-8 2016 DNA-demethylating agent (5-aza-2-deoxy-cytidine (5-aza-CdR)) treatment significantly increased MEG3 expression level in ESCC cells, and TCGA esophageal cancer dataset also showed that DNA methylation of MEG3 predicted survival. Decitabine 25-47 maternally expressed 3 Homo sapiens 203-207 26676363-4 2016 Treatment of glioma cells with the DNA methylation inhibitor 5-Aza-2"-deoxycytidine (5-AzadC) decreased aberrant hypermethylation of the MEG3 promoter and prevented the loss of MEG3 expression. Decitabine 61-83 maternally expressed 3 Homo sapiens 177-181 26676363-4 2016 Treatment of glioma cells with the DNA methylation inhibitor 5-Aza-2"-deoxycytidine (5-AzadC) decreased aberrant hypermethylation of the MEG3 promoter and prevented the loss of MEG3 expression. Decitabine 85-92 maternally expressed 3 Homo sapiens 137-141 26676363-4 2016 Treatment of glioma cells with the DNA methylation inhibitor 5-Aza-2"-deoxycytidine (5-AzadC) decreased aberrant hypermethylation of the MEG3 promoter and prevented the loss of MEG3 expression. Decitabine 85-92 maternally expressed 3 Homo sapiens 177-181 25201080-8 2014 In addition, hypermethylation of MEG3 promoter was identified by methylation-specific PCR and MEG3 expression was robustly increased by the inhibition of methylation with either 5-aza-2-deoxycytidine (5-azadC), or siRNA to DNA methyltransferase 1 (DNMT1) in TGF-beta1-induced LX-2 cells. Decitabine 178-199 maternally expressed 3 Homo sapiens 33-37 26463020-0 2015 [Reversal effect of 5-aza-2-deoxycytidine on the maternally expressed gene 3 promoter hypermethylation and its inhibitory effect on the proliferation of epithelial ovarian cancer cells]. Decitabine 20-41 maternally expressed 3 Homo sapiens 49-76 26463020-1 2015 OBJECTIVE: To investigate the reversal effects of different concentrations of DNA methylation inhibitor, 5-aza-2-deoxycytidine, on the hypermethylation of maternally expressed gene 3 (MEG3) gene promoter, and then the inhibitory effect of restoration of MEG3 expression on the proliferation of ovarian cancer cells. Decitabine 105-126 maternally expressed 3 Homo sapiens 155-182 26463020-1 2015 OBJECTIVE: To investigate the reversal effects of different concentrations of DNA methylation inhibitor, 5-aza-2-deoxycytidine, on the hypermethylation of maternally expressed gene 3 (MEG3) gene promoter, and then the inhibitory effect of restoration of MEG3 expression on the proliferation of ovarian cancer cells. Decitabine 105-126 maternally expressed 3 Homo sapiens 184-188 26463020-6 2015 RESULTS: After treated with 5-aza-2-deoxycytidine, the methylation status of MEG3 in the 0, 1, 5, 10, 20 micromol/L 5-aza-2-deoxycytidine groups were 1.00 +- 0.00, 0.79 +- 0.00, 0.67 +- 0.00, 0.65 +- 0.03 and 0.61 +- 0.01 folds, respectively (P < 0.05 for all). Decitabine 28-49 maternally expressed 3 Homo sapiens 77-81 26463020-6 2015 RESULTS: After treated with 5-aza-2-deoxycytidine, the methylation status of MEG3 in the 0, 1, 5, 10, 20 micromol/L 5-aza-2-deoxycytidine groups were 1.00 +- 0.00, 0.79 +- 0.00, 0.67 +- 0.00, 0.65 +- 0.03 and 0.61 +- 0.01 folds, respectively (P < 0.05 for all). Decitabine 116-137 maternally expressed 3 Homo sapiens 77-81 26463020-7 2015 The relative expressions of MEG3 mRNA in the 0, 1, 5, 10, 20 micromol/L 5-aza-2-deoxycytidine groups were 1.00 +- 0.00, 2.04 +- 0.16, 2.44 +- 0.17, 3.19 +- 0.34 and 5.34 +- 0.39, respectively (P < 0.05 for all). Decitabine 72-93 maternally expressed 3 Homo sapiens 28-32 26463020-10 2015 CONCLUSIONS: Maternally expressed gene 3 promoter hypermethylation is reversed by 5-aza-2-deoxycytidine in ovarian cancer cells. Decitabine 82-103 maternally expressed 3 Homo sapiens 13-40 25201080-8 2014 In addition, hypermethylation of MEG3 promoter was identified by methylation-specific PCR and MEG3 expression was robustly increased by the inhibition of methylation with either 5-aza-2-deoxycytidine (5-azadC), or siRNA to DNA methyltransferase 1 (DNMT1) in TGF-beta1-induced LX-2 cells. Decitabine 178-199 maternally expressed 3 Homo sapiens 94-98 25201080-8 2014 In addition, hypermethylation of MEG3 promoter was identified by methylation-specific PCR and MEG3 expression was robustly increased by the inhibition of methylation with either 5-aza-2-deoxycytidine (5-azadC), or siRNA to DNA methyltransferase 1 (DNMT1) in TGF-beta1-induced LX-2 cells. Decitabine 201-208 maternally expressed 3 Homo sapiens 33-37 25201080-8 2014 In addition, hypermethylation of MEG3 promoter was identified by methylation-specific PCR and MEG3 expression was robustly increased by the inhibition of methylation with either 5-aza-2-deoxycytidine (5-azadC), or siRNA to DNA methyltransferase 1 (DNMT1) in TGF-beta1-induced LX-2 cells. Decitabine 201-208 maternally expressed 3 Homo sapiens 94-98 21625215-6 2011 MEG3 promoter hypermethylation was identified by methylation-specific PCR and MEG3 expression was increased with inhibition of methylation with either 5-Aza-2-Deoxycytidine, or siRNA to DNA Methyltransferase (DNMT) 1 and 3b in HCC cells. Decitabine 151-172 maternally expressed 3 Homo sapiens 0-4 24859196-9 2014 Treatment with 5-aza-2-deoxycytidine reversed the promoter hypermethylation and increased MEG3 expression. Decitabine 15-36 maternally expressed 3 Homo sapiens 90-94 21625215-6 2011 MEG3 promoter hypermethylation was identified by methylation-specific PCR and MEG3 expression was increased with inhibition of methylation with either 5-Aza-2-Deoxycytidine, or siRNA to DNA Methyltransferase (DNMT) 1 and 3b in HCC cells. Decitabine 151-172 maternally expressed 3 Homo sapiens 78-82 30644097-11 2019 More important, hypermethylation of MEG3 promoter could be inhibited by 5-aza-2-deoxycytidine (5-azadC; methylation inhibitor). Decitabine 72-93 maternally expressed 3 Homo sapiens 36-40 30644097-11 2019 More important, hypermethylation of MEG3 promoter could be inhibited by 5-aza-2-deoxycytidine (5-azadC; methylation inhibitor). Decitabine 95-102 maternally expressed 3 Homo sapiens 36-40