Long intergenic noncoding RNA SNHG16 interacts with miR-195 to promote proliferation, invasion and tumorigenesis in hepatocellular carcinoma.

Long non-coding RNAs (lncRNAs) have been confirmed crucial regulators in tumorgenesis. Small nucleolar RNA host gene 16 (SNHG16) has been recently shown to be dysregulated, which uncovered to be a potential oncogene in some cancers. However, the biological function and potential mechanism of SNHG16 in hepatocellular carcinoma (HCC) remain unclear. In our study, our observations showed that the expression level of SNHG16 in HCC tissues and cell lines was upregulated compared with adjacent noncancerous tissues and normal cells. In vitro, loss-of-function experiments revealed that SNHG16 knockdown suppressed the proliferation and weakened invasion of SMMC7721 and HepG2 cells. miR-195 expression was significantly decreased in HCC tissues and negatively correlated with SNHG16 expression. Furthermore, RIP and dual luciferase reporter assays showed that SNHG16 acted as an endogenous sponge by directly binding to miR-195 and downregulated its expression. SNHG16 overexpression inverted the inhibitory effect of miR-195 on proliferation and invasion of SMMC7721 and HepG2 cells. Additionally, SNHG16 depletion resulted in lower tumor growth and weight loss, in vivo. In conclusion, our findings reported that the oncogenic role of SNHG16 in HCC tumorigenesis through a novel SNHG16-miR-195 axis, which provided a novel insight for HCC and helped to probe a potential therapeutic target for the deadly disease.