Title : Acute hypersensitivity of pluripotent testicular cancer-derived embryonal carcinoma to low-dose 5-aza deoxycytidine is associated with global DNA Damage-associated p53 activation, anti-pluripotency and DNA demethylation.

Pub. Date : 2012

PMID : 23300844






5 Functional Relationships(s)
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1 We show here that low-dose 5-aza treatment results in DNA damage and induction of p53 in NT2/D1 cells. Azacitidine tumor protein p53 Homo sapiens
2 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 tumor protein p53 Homo sapiens
3 Changes in the p53 and pluripotency signatures with 5-aza were to a large extent dependent on high levels of DNMT3B. Azacitidine tumor protein p53 Homo sapiens
4 In contrast to the majority of p53 target genes upregulated by 5-aza that did not show DNA hypomethylation, several other genes induced with 5-aza had corresponding decreases in promoter methylation. Azacitidine tumor protein p53 Homo sapiens
5 Our studies suggest that the hypersensitivity of NT2/D1 cells to low-dose 5-aza is multifactorial and involves the combined activation of p53 targets, repression of pluripotency genes, and activation of genes repressed by DNA methylation. Azacitidine tumor protein p53 Homo sapiens