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.

microRNA的失控有助于肝细胞癌（HCC）的异常生长。在这里，我们表明miR-634表达在肝癌中经常降低。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，没有肿瘤包膜和不利的总体生存率显着相关。miR-634的过表达显着减弱了细胞活力，集落形成，肿瘤生长和转移，而miR-634的抑制导致了相反的表型。此外，重新引入的miR-634诱导的细胞凋亡在体外和体内。从机制上讲，miR-634通过直接结合两个基因的3'-UTR来抑制Rab1A和DHX33的表达。在临床样品中，Rab1A或DHX33的表达与miR-634呈负相关。Rab1A或DHX33的重新表达废除了miR-634介导的细胞增殖和迁移抑制作用。总体而言，我们的数据表明miR-634在HCC中具有抑癌作用。新鉴定的miR-634 / Rab1A或miR-634 / DHX33轴可作为临床管理的潜在治疗靶标。