Repression of Dok7 expression mediated by DNMT1 promotes glioma cells proliferation.

In this study, we illustrated that the expression of Dok7 was downregulation in human glioma tissues. Dok7 overexpression significantly inhibits proliferation and colony formation in vitro, and the xenograft tumor formation in vivo. In addition, 5-Aza-2'-deoxycytidine (5-Aza), a DNA methylation inhibitor, preventing the loss of Dok7 expression by decreasing aberrant hypermethylation of Dok7 promoter in glioma cells. More importantly, DNMT1 knockdown induced the demethylation of Dok7 promoter, and enhanced the expression of Dok7 in gliomas. These results suggest that epigenetic silencing of Dok7 may provide a novel glioma treatment strategy.
PMID: 29990858 [PubMed - as supplied by publisher]

Source: Biomedicine and pharmacotherapy = Biomedecine and pharmacotherapie - July 4, 2018 Category: Drugs & Pharmacology Authors: Hua CD, Bian EB, Chen EF, Yang ZH, Tang F, Wang HL, Zhao B Tags: Biomed Pharmacother Source Type: research