LncRNA-SNHG6 promotes the progression of hepatocellular carcinoma by targeting miR-6509-5p and HIF1A

BackgroundAccumulating evidences have been reported that long noncoding RNAs play crucial roles in the progression of hepatocellular carcinoma (HCC). SnoRNA host gene 6 (SNHG6) is believed to be involved in several human cancers, but the specific molecular mechanism of SNHG6 in HCC is not well studied.MethodsIn this study, we experimentally down-regulated the SNHG6 in two hepatocellular carcinoma cell lines in vitro, and then measured the proliferation, migration and invasion abilities and the apoptotic levels. Also, we performed the xenograft assay to investigate the function of SNHG6 during the tumor growth in vivo.ResultsWe found SNHG6 was highly expressed in HCC tissues. Next, using Hep3B and Huh7 cells, we confirmed knockdown of SNHG6 reduced the proliferation, migration and invasion abilities in vitro. Also, by bioinformatics analysis, further molecular and cellular experiments, we found miR-6509-5p bound to SNHG6 directly, and the expression level of HIF1A was regulated through SNHG6/miR-6509-5p axis. Finally, we found that down-regulation of SNHG6 dramatically reduced the tumor growth ability of Huh7 cells in vivo.ConclusionsWe concluded that SNHG6/miR-6509-5p/HIF1A axis functioned in the progression of hepatocellular carcinoma, and could be the promising therapeutic targets during the development of hepatocellular carcinoma drugs.

Automated summary

The study demonstrated that SNHG6 is highly expressed in HCC tissues and knocking down SNHG6 reduces proliferation, migration, and invasion abilities of cells in vitro. The research also revealed the direct binding of miR-6509-5p to SNHG6 and the regulation of HIF1A expression through the SNHG6/miR-6509-5p axis. Furthermore, down-regulation of SNHG6 significantly decreased tumor growth ability of Huh7 cells in vivo, suggesting the potential of SNHG6/miR-6509-5p/HIF1A axis as therapeutic targets for HCC.