MiR-1180 promoted the proliferation of hepatocellular carcinoma cells by repressing TNIP2 expression
作者
Zhou, X;Zhu, HQ;Ma, CQ;Li, HG;Liu, FF;Chang, H;Lu, J
作者单位
[Zhou, Xu; Zhu, Hua-qiang; Ma, Chao-qun; Li, Hong-guang; Liu, Fang-feng; Chang, Hong; Lu, Jun] Shandong Univ, Prov Hosp, Dept Hepatobiliary Surg, 9677 Jingshi Rd, Jinan 250014, Shandong, Peoples R China.
摘要
MicroRNAs (miRNAs) are short, non-coding RNAs with post-transcriptional regulatory function, playing crucial roles in cancer development and progression of hepatocellular carcinoma (HCC). Previous studies have indicated that miR-1180 was implicated in diverse biological processes. However, the underlying mechanism of miR-1180 in HCC has not been intensively investigated. In this study, we aimed to investigate the role of miR-1180 and its target genes in HCC. We found that miR-1180 expression was significantly increased in HCC cells and clinical tissues compared with their corresponding controls. Overexpression of miR-1180 promoted cell proliferation in HCC cell line HepG2. TNFAIP3 interacting protein 2 (TNIP2), a potential target gene of miR-1180, and were validated by a luciferase assay. Further studies revealed that miR-1180 regulated cell proliferation of HCC by directly suppressing TNIP2 expression and the knockdown of TNIP2 expression reversed the effect of miR-1180-in on HCC cell proliferation. In summary, our data indicated that miR-1180 might act as a tumor promoter by targeting TNIP2 during development of HCC. (C) 2016 Elsevier Masson SAS. All rights reserved.
关键词
NF-KAPPA-B; TUMOR-SUPPRESSOR; LIVER-CANCER; ACTIVATION; ANGIOGENESIS; METASTASIS; APOPTOSIS