PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23063977-1 2012 The present study tested whether all-trans retinoic acid (ATRA) and 5-Aza-2"-deoxycitidine (5-Aza) affect AML cell differentiation and growth in vitro by acting on the CCAAT/enhancer binding protein alpha (C/EBPalpha) and c-Myc axis. Azacitidine 68-73 MYC proto-oncogene, bHLH transcription factor Homo sapiens 222-227 25319547-0 2014 5-azacytidine inhibits nonsense-mediated decay in a MYC-dependent fashion. Azacitidine 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 52-55 25319547-5 2014 Moreover, this activity of 5-azacytidine depends on the induction of MYC expression, thus providing a link between the effect of this drug and one of the key cellular pathways that are known to affect NMD activity. Azacitidine 27-40 MYC proto-oncogene, bHLH transcription factor Homo sapiens 69-72 25061731-9 2014 5-Azacytidine suppressed the proliferation of pancreatic cancer cells by inhibiting the Wnt/beta-catenin signaling pathway, particularly the expression of beta-catenin, c-myc, and cyclinD1. Azacitidine 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 169-174 10914736-8 2000 Western blot analyses revealed that 5-aza-CR reactivated p16 expression and repressed c-Myc expression in TSU-PR1 cells but not in DU-145 cells. Azacitidine 36-44 MYC proto-oncogene, bHLH transcription factor Homo sapiens 86-91 23300844-5 2012 Low-dose 5-aza induces a p53 transcriptional signature distinct from that induced with cisplatin in NT2/D1 cells and also uniquely downregulates genes associated with pluripotency including NANOG, SOX2, GDF3 and Myc target genes. Azacitidine 9-14 MYC proto-oncogene, bHLH transcription factor Homo sapiens 212-215 22672838-9 2012 Finally, EMSA and ChIP confirmed that the methylation of the CGCG (-695 to -692) site prevented c-Myc from binding of the site and demethylation treatment of the 5" flanking region of MYCT1 by 5-aza induced the increased occupation of the core promoter by c-Myc (p < 0.01). Azacitidine 193-198 MYC proto-oncogene, bHLH transcription factor Homo sapiens 96-101 22672838-9 2012 Finally, EMSA and ChIP confirmed that the methylation of the CGCG (-695 to -692) site prevented c-Myc from binding of the site and demethylation treatment of the 5" flanking region of MYCT1 by 5-aza induced the increased occupation of the core promoter by c-Myc (p < 0.01). Azacitidine 193-198 MYC proto-oncogene, bHLH transcription factor Homo sapiens 256-261 10914736-10 2000 These findings suggest that 5-aza-CR inhibits telomerase activity via transcriptional repression of hTERT, in which p16 and c-Myc may play a key role. Azacitidine 28-36 MYC proto-oncogene, bHLH transcription factor Homo sapiens 124-129 25487600-0 2015 Overexpression of GYS1, MIF, and MYC is associated with adverse outcome and poor response to azacitidine in myelodysplastic syndromes and acute myeloid leukemia. Azacitidine 93-104 MYC proto-oncogene, bHLH transcription factor Homo sapiens 33-36 34405020-8 2021 5-Aza also increased p53 and p21 transcription through promoter demethylation, and decreased the expression of oncogene c-Myc in 22RV1 and LNCaP cells. Azacitidine 0-5 MYC proto-oncogene, bHLH transcription factor Homo sapiens 120-125 34405020-11 2021 Thus, in responsible for its apoptotic induction and DNA damage, the mechanism of the antitumor activities of 5-Aza may involve in an increase of tumor suppressive maspin, upregulation of wild type p53-mediated p21 expression and a decrease of oncogene c-Myc level in 22RV1 and LNCaP cells, and enhancing the tumor suppressive maspin expression in DU145 cells. Azacitidine 110-115 MYC proto-oncogene, bHLH transcription factor Homo sapiens 253-258 2425967-0 1986 Methylation and expression of c-myc and c-abl oncogenes in human leukemic K562 cells before and after treatment with 5-azacytidine. Azacitidine 117-130 MYC proto-oncogene, bHLH transcription factor Homo sapiens 30-35 34837933-9 2021 In addition, mRNA analyses demonstrated that MOLT4 and jurkat cells, expressed p53 gene more than 10-fold higher compared with untreated cells in three independent experiments while the cells suppressed the expression of a subset of functionally related genes including MYC, BCL2, APEX, SIRT1, SNAIL1 and vimentin to some extent, following 5-AZA treatment. Azacitidine 340-345 MYC proto-oncogene, bHLH transcription factor Homo sapiens 270-273