PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25502084-10 2015 Treatment with the chemotherapeutic agent decitabine, a known DNA methyltransferase inhibitor, increased miR-200c/141 expression and ameliorated decreased expression of miR-200c/141 induced by TGF-beta in SGC-7901 cells. Decitabine 42-52 transforming growth factor beta 1 Homo sapiens 193-201 25502084-11 2015 Our study revealed that miR-200c/141 was downregulated by CpG island methylation and TGF-beta signaling, which decreased ZEB1/2 expression and increased E-cadherin expression to inhibit migration and invasion of gastric cancer cells and provides powerful evidence for the application of decitabine in gastric cancer treatment. Decitabine 287-297 transforming growth factor beta 1 Homo sapiens 85-93 25003579-9 2014 Computational findings were substantiated by experimental validation of expression of key genes involved in two critical pathways affected by decitabine (TGF-beta and Hh). Decitabine 142-152 transforming growth factor beta 1 Homo sapiens 154-162 28802229-6 2017 Addition of 5-AzadC also reduced the TGF-beta-stimulated proliferation, migration and invasiveness of glioma cells. Decitabine 12-19 transforming growth factor beta 1 Homo sapiens 37-45 25860431-8 2014 After the intervention with 5-aza-2-deoxycytidine in the K+ group, the expression of DNMT1 and TGF-beta1 mRNA was lower, Smad7 mRNA was elevated in pathological scar fibroblasts, the flow cytometry showed the proportion of cells in G0/G1 phase were increased, and the proportion of apoptosis cells were also increased, with similar changes in the cells in the H and H+ groups. Decitabine 28-49 transforming growth factor beta 1 Homo sapiens 95-104 18292494-5 2008 Furthermore, treatment of T cells with either TGF-beta or UO126 significantly down-regulated the expression of DNMTs, a reaction normally elicited by demethylation agents, such as 5-Aza-2"-deoxycytidine. Decitabine 180-202 transforming growth factor beta 1 Homo sapiens 46-54 24228511-0 2013 [Effect of the methylation enzyme inhibitors of 5-aza-2-deoxycytidine on the TGF-beta/smad signal transduction pathway in human keloid fibroblasts]. Decitabine 48-69 transforming growth factor beta 1 Homo sapiens 77-85 24228511-1 2013 OBJECTIVE: To investigate the effect of 5-aza-2-deoxycytidine on the TGF-beta/smad signal transduction pathway in human keloid fibroblasts (KFSs). Decitabine 40-61 transforming growth factor beta 1 Homo sapiens 69-77 24228511-10 2013 CONCLUSIONS: 5-aza-2-deoxycytidine, methylase inhibitors, inhibits cell proliferation and promotes apoptosis of KFSs, which may be associated with the suppression of TGF-beta/smad signal pathway. Decitabine 13-34 transforming growth factor beta 1 Homo sapiens 166-174 15905358-3 2005 Sensitivity to TGF-beta was restored in cells treated with 5-Aza-2"-deoxycytidine (5-Aza), as indicated by an increase in the expression of phosphorylated Smad-2, type I (TbetaRI), and type II (TbetaRII) TGF-beta receptors, and a reduced rate of proliferation. Decitabine 59-81 transforming growth factor beta 1 Homo sapiens 15-23 15905358-3 2005 Sensitivity to TGF-beta was restored in cells treated with 5-Aza-2"-deoxycytidine (5-Aza), as indicated by an increase in the expression of phosphorylated Smad-2, type I (TbetaRI), and type II (TbetaRII) TGF-beta receptors, and a reduced rate of proliferation. Decitabine 59-81 transforming growth factor beta 1 Homo sapiens 204-212 9632722-0 1998 Induction of transforming growth factor-beta receptor type II expression in estrogen receptor-positive breast cancer cells through SP1 activation by 5-aza-2"-deoxycytidine. Decitabine 149-171 transforming growth factor beta 1 Homo sapiens 13-44 9632722-10 1998 These results indicate that the transcriptional repression of RII in the ER+ breast cancer cells is caused by suboptimal activity of Sp1, whereas treatment with 5-aza-2"-dC stabilizes the protein thus increasing steady-state Sp1 levels and thereby leads to enhanced RII transcription and subsequent restoration of TGF-beta sensitivity. Decitabine 161-172 transforming growth factor beta 1 Homo sapiens 314-322 34890285-6 2022 Our results suggested that TGF-beta1 stimulates the phosphorylation levels of ERK1/2 and p38 via increasing TGFBI expression, TGFBI-MAPK signaling pathway plays an important role in the synergy of DAC and CDDP against UC. Decitabine 197-200 transforming growth factor beta 1 Homo sapiens 27-36 29843383-5 2018 Here, we show that treatment of PC3 prostate cancer cells with the DNA methyltransferase (DNMT) inhibitor decitabine demethylates the DKK3 promoter, induces DKK3 expression, and inhibits TGF-beta/Smad-dependent transcriptional activity. Decitabine 106-116 transforming growth factor beta 1 Homo sapiens 187-195 29555582-5 2018 We found that COX-2 protein expression and PGE2 production were markedly reduced by TGF-beta1 and this was prevented by the pan-histone deacetylase inhibitor suberanilohydroxamic acid (SAHA) and to a lesser extent by the DNA demethylating agent Decitabine (DAC), but not by the G9a histone methyltransferase (HMT) inhibitor BIX01294 or the EZH2 HMT inhibitor 3-deazaneplanocin A (DZNep). Decitabine 245-255 transforming growth factor beta 1 Homo sapiens 84-93 29555582-5 2018 We found that COX-2 protein expression and PGE2 production were markedly reduced by TGF-beta1 and this was prevented by the pan-histone deacetylase inhibitor suberanilohydroxamic acid (SAHA) and to a lesser extent by the DNA demethylating agent Decitabine (DAC), but not by the G9a histone methyltransferase (HMT) inhibitor BIX01294 or the EZH2 HMT inhibitor 3-deazaneplanocin A (DZNep). Decitabine 257-260 transforming growth factor beta 1 Homo sapiens 84-93 29456534-5 2018 This hurdle can be potentially overcome by pharmacological interference with DNA methyltransferase activity and CpG methylation [e.g., by the cytosine nucleoside analog 5-aza-2"-deoxycytidine (5-aza-dC)] to stabilize TGF-beta-induced Foxp3 expression and to promote a Foxp3+ iTreg cell phenotype even in the absence of added TGF-beta. Decitabine 169-191 transforming growth factor beta 1 Homo sapiens 217-225 29456534-5 2018 This hurdle can be potentially overcome by pharmacological interference with DNA methyltransferase activity and CpG methylation [e.g., by the cytosine nucleoside analog 5-aza-2"-deoxycytidine (5-aza-dC)] to stabilize TGF-beta-induced Foxp3 expression and to promote a Foxp3+ iTreg cell phenotype even in the absence of added TGF-beta. Decitabine 169-191 transforming growth factor beta 1 Homo sapiens 325-333 28405157-0 2017 Decitabine reverses TGF-beta1-induced epithelial-mesenchymal transition in non-small-cell lung cancer by regulating miR-200/ZEB axis. Decitabine 0-10 transforming growth factor beta 1 Homo sapiens 20-29 28435228-0 2017 Erratum: Decitabine reverses TGF-beta1-induced epithelial-mesenchymal transition in non-small-cell lung cancer by regulating miR-200/ZEB axis [Corrigendum]. Decitabine 9-19 transforming growth factor beta 1 Homo sapiens 29-38 28405157-4 2017 METHODS: In this study, we determined the effect of decitabine, a DNA methyltransferase inhibitor, on TGF-beta1-induced EMT in non-small-cell lung cancer (NSCLC) PC9 and A549 cells. Decitabine 52-62 transforming growth factor beta 1 Homo sapiens 102-111 28405157-6 2017 RESULTS: Decitabine reversed TGF-beta1-induced EMT in PC9 cells, but not in A549 cells. Decitabine 9-19 transforming growth factor beta 1 Homo sapiens 29-38