Abstract
Laryngeal squamous cell carcinoma (LSCC) is a common malignancy of the head and neck. Long noncoding RNAs (lncRNAs) play essential roles in the development and treatment of LSCC. However, the role and regulatory mechanism of lncRNA small nucleolar RNA host gene 3 (SNHG3) in LSCC progression remain largely unknown. Twenty-five paired LSCC tissues and normal samples were collected. The expression levels of SNHG3, Yes-associated protein 1 (YAP1), and microRNA-340-5p (miR-340-5p) were measured via quantitative real-time polymerase chain reaction or western blot. Cell viability, apoptosis, and glycolysis were investigated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide, flow cytometry, and specific assay kit, respectively. The association between SNHG3 and miR-340-5p or miR-340-5p and YAP1 was assessed by dual-luciferase reporter assay. The expression of a protein involved in the Wnt/β-catenin pathway was detected by western blot. The xenograft model was established to assess the anti-cancer role of SNHG3 inhibition in vivo. We found that the levels of SNHG3 and YAP1 were increased but the miR-340-5p expression was decreased in LSCC tissues and cells. The knockdown of SNHG3 or YAP1 inhibited cell viability and glycolysis but induced apoptosis in LSCC cells. Overexpression of YAP1 reversed the effect of SNHG3 knockdown on LSCC progression. SNHG3 could regulate YAP1 expression by competitively binding with miR-340-5p. Overexpression of miR-340-5p suppressed cell viability and glycolysis but promoted apoptosis in LSCC cells. Knockdown of SNHG3 repressed Wnt/β-catenin pathway by regulating miR-340-5p and YAP1. The silencing of SNHG3 reduced LSCC xenograft tumor growth. In conclusion, knockdown of SNHG3 inhibited LSCC progression via inactivating Wnt/β-catenin pathway by regulating the miR-340-5p/YAP1 axis.