MiR-545-3p/MT1M axis regulates cell proliferation, invasion and migration in hepatocellular carcinoma

IF 7.5 2区 医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL Biomedicine & Pharmacotherapy Pub Date : 2018-12-01 DOI:10.1016/j.biopha.2018.09.009
Liu Changjun , Huang Feizhou , Peng Dezhen , Lei Zhao , Mao Xianhai
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引用次数: 41

Abstract

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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MiR-545-3p/MT1M轴调控肝癌细胞增殖、侵袭和迁移
研究表明,金属硫蛋白1m (metallothionein 1m, MT1M)是一种肿瘤抑制基因,在人肝细胞癌(HCC)中经常下调。MT1M启动子区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,我们发现我们队列中55个HCC肿瘤组织中仍有一半不具有MT1M启动子甲基化。因此,我们推测可能有其他机制参与了MT1M在HCC中的下调。然后,我们提供证据表明,作为肿瘤启动子的miR-545-3p通过结合其非翻译区(3'UTR)对HCC中的MT1M进行转录后调控。综上所述,我们研究了miR-545-3p通过调节MT1M在HCC过程中的作用。
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来源期刊
CiteScore
11.90
自引率
2.70%
发文量
1621
审稿时长
48 days
期刊介绍: Biomedicine & Pharmacotherapy stands as a multidisciplinary journal, presenting a spectrum of original research reports, reviews, and communications in the realms of clinical and basic medicine, as well as pharmacology. The journal spans various fields, including Cancer, Nutriceutics, Neurodegenerative, Cardiac, and Infectious Diseases.
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