肝细胞癌
下调和上调
甲基化
癌症研究
发起人
非翻译区
DNA甲基化
生物
抑癌基因
抑制器
三素数非翻译区
细胞生长
基因
基因表达
信使核糖核酸
癌变
遗传学
作者
Liu Changjun,Huang Feizhou,Dezhen Peng,Lei Zhao,Mao Xianhai
标识
DOI:10.1016/j.biopha.2018.09.009
摘要
Studies have shown that metallothionein 1 M (MT1M) is a tumor suppressor gene which is frequently down-regulated in human hepatocellular carcinoma (HCC). The methylation of MT1M promoter region is one of the important transcriptional regulation mechanisms that contribute to the loss of its expression. In our study, we found that there are still half of the 55 HCC tumor tissues in our cohort do not share the promoter methylation of MT1M. So, we speculated there maybe another mechanism participating in the downregulation of MT1M in HCC. Then, we provided evidences that miR-545-3p, which served as a tumor promoter, post-transcriptionally regulate MT1M in HCC through binding to its untranslated region (3'UTR). Taking together, we investigated the role of miR-545-3p in the process of HCC through regulating MT1M.
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