LncRNA SNHG20 enhances the progression of oral squamous cell carcinoma by regulating the miR-29a/DIXDC1/Wnt regulatory axis.

Abstract

Oral squamous cell carcinoma (OSCC) comprises approximately ~90% of all oral malignancies and exhibits a significant mortality rate worldwide. Although the dysregulation of small nucleolar RNA host gene 20 (SNHG20) participates in the development of multiple malignancies, the molecular mechanisms underlying its regulation of OSCC progression remain to be fully elucidated. The expression levels of SNHG20, microRNA-29a (miR-29a), and Disheveled-Axin Domain Containing 1 (DIXDC1) were detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). The protein expression levels of DIXDC1 and β-catenin were measured by Western blotting. In addition, MTT assay was performed to measure the cell proliferation ability in SCC9 and SCC15 cells. Cell migration and invasion abilities were measured by wound healing assay and transwell assay, respectively. The cell apoptosis was assessed by flow cytometry assay. Besides, Luciferase reporter assay was employed to examine the interrelation between miR-29a and SNHG20 or DIXDC1. It was demonstrated that SNHG20 and DIXDC1 were significantly upregulated in OSCC tissues and cell lines, while miR-29a was markedly downregulated. Moreover, the high expression of SNHG20 was found to predict a lower survival rate in OSCC patients. In addition, loss-of-function experiments demonstrated that SNHG20 knockdown inhibited the development and progression of OSCC, whereas the miR-29a inhibitor significantly abolished the effect of SNHG20 depletion on OSCC progression by directly binding to SNHG20. DIXDC1 was shown to enhance si-SNHG20 and miR-29a mimic-attenuated cell viability, migration, and invasion by directly binding to miR-29a. Furthermore, it was also found that DIXDC1 activated Wnt signaling in OSCC cells. Our study demonstrated that SNHG20 promoted OSCC progression via the miR-29a/DIXDC1/Wnt signaling pathway, which might provide a novel theoretical basis for the treatment of OSCC.