Anticancer drugs induce hypomethylation of the acetylcholinesterase promoter via a phosphorylated-p38-DNMT1-AChE pathway in apoptotic hepatocellular carcinoma cells.
作者： Qiliang Xi , Ning Gao , Yang Yang , Weiyuan Ye , Bo Zhang
DOI: 10.1016/J.BIOCEL.2015.08.013
关键词: Molecular biology 、 Methyltransferase 、 Acetylcholinesterase 、 Apoptosis 、 Programmed cell death 、 Cisplatin 、 Gene silencing 、 Cancer research 、 RNA interference 、 Biology 、 Signal transduction
摘要: Apoptosis, also known as programmed cell death, plays an essential role in eliminating excessive, damaged or harmful cells. Previous work has demonstrated that anticancer drugs induce apoptosis by inducing cytotoxicity. In recent years, several reports modulated expression of DNA methyltransferases 1 (DNMT1) and acetylcholinesterase (AChE) a variety tumors. this study, we showed the DNMT1 was decreased methylation CpGs promoter AChE reduced drugs-induced apoptotic hepatocellular carcinoma Silencing AZA RNA interference (RNAi) restored production inhibition RNAi protected HCC cells from apoptosis. Furthermore, regulation involved phosphorylated p38 pathway addition, immunohistochemical staining P-p38, were aberrantly expressed subset Taken together, further, found
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