Downregulation of long noncoding RNA TINCR inhibits cell proliferation, invasion, and epithelial-mesenchymal transition of hepatocellular carcinoma

Abstract

Accumulating reports have identified that long non-coding RNAs (lncRNAs) function as key regulators of tumor initiation and progression. The aim of the current study was to determine the clinical significance and functional role of TINCR in hepatocellular carcinoma (HCC). In the present study, the level of lncRNA TINCR expression was significantly upregulated in HCC tissues compared to adjacent normal tissues. Higher levels of lncRNA TINCR expression were significantly correlated with tumor size and vascular invasion of HCC patients. LncRNA TINCR knockdown inhibited cell proliferation ability, increased the proportion of G1 phase cells, reduced the proportion of S phase cells, and suppressed cell invasion of HCC in vitro. Additionally, lncRNA TINCR knockdown inhibited the HCC cell epithelial-mesenchymal transition (EMT) phenomenon by upregulating E-cadherin and reducing N-cadherin expression. We demonstrated that knockdown of lncRNA reduced tumor growth in vivo. Thus, these results indicated that lncRNA TINCR exhibits a tumor oncogenic role in HCC and inhibition of lncRNA TINCR might serve as a therapeutic target for HCC.