Acta2 Promotes Epithelial-Mesenchymal Transition In OSCC

This study investigates the role of ACTA2 overexpression at the invasive front of oral squamous cell carcinoma (OSCC) in modulating tumor cell behavior and progression. Digital Spatial Profiling(DSP) technology screened abnormally expressed molecules at OSCC invasive fronts. TCGA database analysis compared ACTA2 levels between metastatic and non-metastatic OSCC. Clinical OSCC samples were validated via RT-PCR and Western blot. Lentiviral transfection established ACTA2-overexpressing OSCC cell lines. Functional assays (scratch wound, CCK8, colony formation, Transwell migration/invasion) evaluated in vitro behaviors. Xenograft and pulmonary metastasis mouse models assessed in vivo tumor growth and metastasis. Western blot analyzed epithelial-mesenchymal transition (EMT) markers. ACTA2 expression was significantly elevated at the invasive front of metastatic tumors compared to non-metastatic counterparts, a finding corroborated by TCGA database analysis and immunohistochemical validation in clinical OSCC specimens. Overexpression of ACTA2 enhanced OSCC cell proliferation, migration, invasion, and colony-forming capabilities in vitro. Concurrently, it induced epithelial-mesenchymal transition (EMT) progression, characterized by reduced epithelial marker (E-cadherin) expression and increased mesenchymal markers (N-cadherin, Vimentin) and transcription factor Snail levels. In vivo experiments demonstrated that ACTA2 overexpression promoted tumor growth and pulmonary metastasis in xenograft models. ACTA2 overexpression at OSCC invasive fronts drives tumor progression by inducing EMT.