Tra2β exerts tumor-promoting effects via GSK3/β-catenin signaling in oral squamous cell carcinoma.

Abstract

The splicing factor transformer-2 homolog beta (Tra2β) plays a pivotal role in various cancers. Nonetheless, its role in oral squamous cell carcinoma (OSCC) has not been comprehensively explored. This study sought to discern the influence of Tra2β on OSCC and its underlying mechanisms. We assessed Tra2β expression in OSCC utilizing immunohistochemistry, qRT-PCR, and western blotting techniques. siRNA transfection was used to silence Tra2β. Whole transcriptome RNA sequencing (RNA-seq) analysis was carried out to reveal the alternative splicing (AS) events. KEGG pathway analysis enriched the related pathways. Colony formation, transwell, wound healing, and Annexin V-FITC/PI were employed to appraise the consequences of Tra2β silencing on OSCC. Tra2β was highly expressed in both OSCC tissues and cell lines. Knockdown of Tra2β-regulated AS events with skipped exon (SE) accounts for the highest proportion. Meanwhile, downregulation of Tra2β reduced cell proliferation, migration, and invasion, however increasing cell apoptosis. Moreover, Wnt signaling pathway involved in the function of Tra2β knockdown which was demonstrated directly by a discernible reduction in the expression of GSK3/β-catenin signaling axis. These findings suggest that knockdown of Tra2β may exert anti-tumor effects through the GSK3/β-catenin signaling pathway in OSCC.