SNHG16 promotes hepatocellular carcinoma development via activating ECM receptor interaction pathway.

Abstract Background Accumulating data have suggested that long non-coding RNAs (lncRNAs) play important roles in regulating tumor cell growth. This study was designed to investigate the role of SNHG16 in hepatocellular carcinoma (HCC). Methods SNHG16 expression was detected with real-time polymerase chain reaction (PCR). The cutoff value of SNHG16 for tumor-free survival (TFS) was determined with receiver operating characteristic curve analysis. Small interfering RNA was used to inhibit the expression of SNHG16 in HCC cell lines. The biologic behavior of HCC cell was determined with cell viability assay and Transwell assay in vitro. The potential predictive value of SNHG16 on prognosis was analyzed by Kaplan-Meier curves and Cox proportional hazards regression model. Results SNHG16 expression was upregulated in tumor tissues and HCC cell lines. High expression of SNHG16 was associated with tumor recurrence and poor prognosis after surgery. Multivariate analysis revealed that SNHG16 was an independent prognostic factor for poor recurrence-free survival. Moreover, inhibition of SNHG16 in HepG2, Hep3B, and BEL-7402 cells significantly reduced cell invasiveness and proliferation. Mechanistic analyses indicated that the ECM-receptor interaction pathway was remarkably activated by SNHG16. Conclusions SNHG16 might be a promising biomarker for predicting tumor recurrence in HCC patients after surgery and a potential therapeutic target for HCC.