Upregulation of lncRNA Sox2ot indicates a poor prognosis for patients with hepatocellular carcinoma and promotes cell invasion.

Abstract

Long non-coding RNA Sox2 overlapping transcript (lncRNA Sox2ot) expression has been demonstrated to be upregulated in a number of types of tumor, and may act as an oncogene. The present study aimed to evaluate the clinical role of lncRNA Sox2ot and its association with the epithelial-mesenchymal transition in hepatocellular carcinoma (HCC). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to determine the expression of lncRNA Sox2ot in 86 cases of HCC tissues and adjacent non-tumor tissues. Kaplan-Meier and log-rank test was used to analyze the association between lncRNA Sox2ot expression and disease-free (DFS) or overall (OS) survival time. In addition, the capacity of HCC cells with lncRNA Sox2ot knockdown for invasion was evaluated via transwell cell invasion assays. RT-qPCR and western blot analyses were also performed to determine the mRNA and protein expression of Twist1, E-cadherin and N-cadherin in the HCC cells. It was indicated that lncRNA Sox2ot expression levels were significantly higher in HCC tissues compared with adjacent non-tumor tissues. Increased expression levels of lncRNA Sox2ot were associated with the tumor size, the tumor number and vein invasion in patients with HCC. An association was observed between lncRNA Sox2ot and the DFS and OS of patients with HCC. Furthermore, it was determined that cell invasion was inhibited following the siRNA knockdown of lncRNA Sox2ot in MHCC97H and SMCC-7721 cells via transwell cell invasion assays. Furthermore, it was demonstrated that knockdown of lncRNA Sox2ot downregulated the mRNA and protein expression of Twist1 and N-cadherin, but upregulated the E-cadherin expression levels in MHCC97H and SMCC-7721 cells. Thus, it was indicated that lncRNA Sox2ot may be a novel predictive biomarker and a potential therapeutic target for HCC.