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miR-634通过Rab1A和DHX33对肝细胞癌表现出抗肿瘤活性。

miR-634 exhibits anti-tumor activities toward hepatocellular carcinoma via Rab1A and DHX33.

作者信息

Zhang Chris Zhiyi, Cao Yun, Fu Jia, Yun Jing-Ping, Zhang Mei-Fang

机构信息

Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China; Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou 510060, China.

Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China; Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou 510060, China.

出版信息

Mol Oncol. 2016 Dec;10(10):1532-1541. doi: 10.1016/j.molonc.2016.09.001. Epub 2016 Sep 20.

DOI:10.1016/j.molonc.2016.09.001
PMID:27693040
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5423132/
Abstract

Deregulation of microRNAs contributes to the aberrant growth of hepatocellular carcinoma (HCC). Here, we showed that miR-634 expression was frequently decreased in HCC. Low miR-634 expression was significantly associated with larger tumor size, poorer tumor differentiation, advanced TNM stage, vascular invasion, absence of tumor capsule and unfavorable overall survival. Overexpression of miR-634 markedly attenuated cell viability, colony formation, tumor growth and metastasis, whereas miR-634 inhibition resulted in the opposite phenotypes. Furthermore, re-introduction of miR-634 induced cell apoptosis in vitro and in vivo. Mechanistically, miR-634 inhibited the expression of Rab1A and DHX33 via directly binding to the 3'-UTR of both genes. In clinical samples, the expression of Rab1A or DHX33 was reversely correlated with miR-634. Re-expression of Rab1A or DHX33 abrogated the miR-634-mediated inhibition of cell proliferation and migration. Collectively, our data suggest a tumor suppressor role of miR-634 in HCC. The newly identified miR-634/Rab1A or miR-634/DHX33 axis serves as a potential therapeutic target for the clinical management.

摘要

微小RNA的失调促成了肝细胞癌（HCC）的异常生长。在此，我们表明miR-634在HCC中表达常常降低。低miR-634表达与更大的肿瘤大小、更差的肿瘤分化、晚期TNM分期、血管侵犯、无肿瘤包膜以及不良的总生存期显著相关。miR-634的过表达显著减弱细胞活力、集落形成、肿瘤生长和转移，而miR-634抑制则导致相反的表型。此外，重新引入miR-634在体外和体内均诱导细胞凋亡。机制上，miR-634通过直接结合Rab1A和DHX33两个基因的3'-UTR来抑制其表达。在临床样本中，Rab1A或DHX33的表达与miR-634呈负相关。Rab1A或DHX33的重新表达消除了miR-634介导的对细胞增殖和迁移的抑制。总体而言，我们的数据表明miR-634在HCC中起肿瘤抑制作用。新鉴定出的miR-634/Rab1A或miR-634/DHX33轴可作为临床治疗的潜在靶点。

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