LINC00152 promotes cell cycle progression in hepatocellular carcinoma via miR-193a/b-3p/CCND1 axis. Issue 8 (18th April 2018)

• Record Type: Journal Article
• Authors: Ma, Pei; Wang, Haitao; Sun, Jiangyang; Liu, Hongzhou; Zheng, Chao; Zhou, Xin; Lu, Zhongxin
• Is Part Of: Cell cycle. Volume 17:Issue 8(2018)
• Page Start: 974
• Page End: 984
• Publication Date: 2018-04-18
• Subjects: Hepatocellular carcinoma -- LINC00152 -- miR-193a/b-3p -- CCND1 -- cell cycle; Cell cycle -- Periodicals; 571.84377
• DOI: 10.1080/15384101.2018.1464834
• Languages: English
• ISSNs: 1538-4101

Abstract

ABSTRACT: Long intergenic non-coding RNA 00152 (LINC00152) is aberrantly expressed in various human malignancies and plays an important role in the pathogenesis. Here, we found that LINC00152 is upregulated in hepatocellular carcinoma (HCC) tissues as compared to adjacent non-neoplastic tissues; gain-and-loss-of-function analyses in vitro showed that LINC00152 facilitates HCC cell cycle progression through regulating the expression of CCND1. LINC00152 knockdown inhibits tumorigenesis in vivo. MS2-RIP analysis indicated that LINC00152 binds directly to miR-193a/b-3p, as confirmed by luciferase reporter assays. Furthermore, ectopic expression of LINC00152 partially halted the decrease in CCND1 expression and cell proliferation capacity induced by miR-193a/b-3p overexpression. Thus, LINC00152 acts as a competing endogenous RNA (ceRNA) by sponging miR-193a/b-3p to modulate its target gene, CCND1. Our findings establish a ceRNA mechanism regulating cell proliferation in HCC via the LINC00152/miR-193a/b-3p/CCND1 signalling axis, and identify LINC00152 as a potential therapeutic target for HCC.