LINC01018 confers a novel tumor-suppressor role in hepatocellular carcinoma through sponging microRNA-182-5p.

Hepatocellular carcinoma (HCC) is the second leading cause of the cancer-related mortality. Emerging evidence has demonstrated that some long non-coding RNAs (lncRNAs) are involved in the development and progression of HCC. Herein, the current study aimed to explore the potential mechanism of LINC01018 in regulating the progression of HCC. Initially, the expression of LINC01018, microRNA-182-5p (miR-182-5p), and forkhead box protein O1 (FOXO1) was quantified in 72 paired HCC and adjacent normal tissue samples, as well as HCC cells, followed by the identification of the interaction among them. In order to define the contributory role of LINC01018 in the progression of HCC, the expression of LINC01018, miR-182-5p, or FOXO1 was altered in HCC cells, followed by the evaluation of cell proliferation, cell cycle distribution, and cell apoptosis. Finally, in vivo tests were performed to further verify the role of LINC01018 in HCC. It was observed that LINC01018 and FOXO1 were poorly expressed but miR-182-5p was highly expressed in HCC tissues and cells. The up-regulation of LINC01018 was shown to decrease proliferation while promoting apoptosis of HCC cells. LINC01018 acted as a sponge of miR-182-5p, which targeted FOXO1. At last, mice injected with Hep3B over-expressing FOXO1 displayed suppressed xenograft tumor formation. Collectively, over-expression of LINC01018 represses proliferation and promotes apoptosis of HCC cells via up-regulation of FOXO1 by sponging miR-182-5p, which highlights over-expression of LINC01018 as a candidate suppressor of HCC.