LncRNA DLX6-AS1 promotes laryngeal squamous cell carcinoma growth and invasion through regulating miR-376c.

Accumulating evidence showed that lncRNAs play important roles in tumour development. Recently, a novel lncRNA DLX6-AS1 was found to be overexpressed in some tumors such as lung adenocarcinoma, renal cell carcinoma and hepatocellular carcinoma. However, the functional roles of DLX6-AS1 in laryngeal squamous cell carcinoma (LSCC) are still unclear. In the study, we showed that the expression level of DLX6-AS1 was upregulated in the LSCC samples compared to the noncancerous tissues. By using CCK-8 analysis, we demonstrated that knockdown expression of DLX6-AS1 suppressed the Hep2 cell growth. DLX6-AS1 knockdown inhibited the Hep2 cell cycle and invasion. MiR-376c was identified to have the complementary binding sites with the DLX6-AS1. By luciferase reporter assay, we indicated that overexpression of miR-376c inhibited the luciferase activity of wild-type DLX6-AS1, but it failed to suppress luciferase activity of mutated one. DLX6-AS1 knockdown enhanced the expression of miR-376c in the Hep2 cell. Moreover, we showed that the expression level of miR-376c was lower in the LSCC samples than in the noncancerous tissues and the expression of miR-376c was negatively correlated with expression of DLX6-AS1 in LSCC tissues. Ectopic expression of miR-376c suppressed cell proliferation, cycle and invasion of LSCC cell. DLX6-AS1 knockdown suppressed cell proliferation, cycle and invasion via regulating miR-376c expression. These data proved that lncRNA DLX6-AS1 might play as an oncogene in LSCC development and tumorigenesis.