LncRNA SNHG16 promotes proliferation and migration in laryngeal squamous cell carcinoma via the miR-140–5p/NFAT5/Wnt/β-catenin pathway axis

Abstract

BackgroundRecent studies demonstrate that long noncoding RNAs (lncRNAs) are involved in the development of various cancers. Many lncRNAs were reported to abnormally express in laryngeal squamous cell carcinoma (LSCC) and play pivotal roles in its development. LncRNA small nucleolar RNA host gene 16 (SNHG16) was previously validated as an oncogene in hepatocellular carcinoma. Nevertheless, the biological role of SNHG16 in LSCC still needs more explorations. The goal of this assay is to explore the function and molecular mechanism of lncRNA SNHG16 in the development of LSCC. Methods and resultsFirst, RT-qPCR demonstrated the upregulation of SNHG16 in LSCC cells and tissues. Loss-of-function assays determined the inhibitive influence of SNHG16 downregulation on cell viability, growth, and migration in LSCC. Furthermore, SNHG16 bound with miR-140–5p in LSCC. MiR-140–5p overexpression suppressed LSCC cell proliferation and migration. NFAT5 was identified as a direct target of miR-140–5p. Through rescue experiments, overexpression of NFAT5 reversed SNHG16 knockdown-mediated suppression on cell viability, growth, and migration in LSCC. Additionally, NFAT5 overexpression activated while NFAT5 downregulation inhibited the Wnt/β-catenin signaling pathway. ConclusionLncRNA SNHG16 is upregulated in LSCC and contributes to the development of LSCC via regulating the miR-140–5p/NFAT5/Wnt/β‐catenin pathway axis. The SNHG16/miR-140–5p/NFAT5/Wnt/β‐catenin pathway axis might provide a novel strategy for LSCC treatment.