Knockdown of long non-coding RNA LINC01006 represses the development of hepatocellular carcinoma by modulating the miR-194-5p/CADM1 axis

Abstract

Introduction and objectivesLong non-coding RNAs (lncRNAs) have great potential as therapeutic targets in hepatocellular carcinoma (HCC). In this study, we aimed to uncover the function and molecular mechanism of long intergenic non-protein coding RNA 1006 (LINC01006) in HCC. Materials and methodsMice were injected with HCC cells in order to establish the HCC model. Quantitative reverse transcription polymerase chain reaction was used to determine the expression levels of LINC01006, cell adhesion molecule 1 (CADM1), and microRNA (miR)-194-5p in HCC tissues and cells. The cell proliferation, invasion, and migration abilities were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide, transwell, and wound healing assays. The interrelation between LINC01006, miR-194-5p, and CADM1 was confirmed by a dual-luciferase reporter assay. Western blotting was employed to assess the relative protein expression level of CADM1. ResultsLINC01006 and CADM1 displayed upregulation, but miR-194-5p exhibited downregulation in HCC cells and tissues. Short hairpin (sh)-LINC01006 and miR-194-5p mimics repressed the proliferative, migratory, and invasive capacities of HCC cells, and injection of sh-LINC01006 restrained the growth of HCC tumours in mice. LINC01006 served as a competing endogenous RNA of miR-194-5p and was inversely correlated with miR-194-5p. CADM1 was targeted by miR-194-5p, inversely correlated with miR-194-5p, and positively associated with LINC01006. Furthermore, transfection of pcDNA-CADM1 or the miR-194-5p inhibitor reversed the suppressive effects of sh-LINC01006 on the proliferation, invasion, and migration abilities of HCC cells. ConclusionsDownregulation of LINC01006 repressed the development of HCC by sponging miR-194-5p to modulate the expression of CADM1, implying its potential as a therapeutic target for HCC.