Department of Hepatobiliary Surgery, Hunan People's Hospital, Changsha 410005, China; Department of General surgery, the Third Xiangya Hospital of Central South University, Changsha 410013, China.
Department of General surgery, the Third Xiangya Hospital of Central South University, Changsha 410013, China.
Biomed Pharmacother. 2018 Dec;108:347-354. doi: 10.1016/j.biopha.2018.09.009. Epub 2018 Sep 15.
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.
研究表明，金属硫蛋白 1M（MT1M）是一种肿瘤抑制基因，在人肝癌（HCC）中经常下调。MT1M 启动子区域的甲基化是导致其表达缺失的重要转录调控机制之一。在我们的研究中，我们发现我们的队列中仍有一半的 55 个 HCC 肿瘤组织不具有 MT1M 启动子甲基化。因此，我们推测在 HCC 中可能存在另一种参与 MT1M 下调的机制。然后，我们提供了证据表明，miR-545-3p 作为一种肿瘤促进剂，通过与 MT1M 的非翻译区（3'UTR）结合，在 HCC 中进行转录后调控 MT1M。总之，我们通过调节 MT1M 研究了 miR-545-3p 在 HCC 过程中的作用。
