Bcl-2 and Twist1 can be coactivated by hypoxia in hepatocellular carcinoma to promote tumor cell metastasis and vasculogenic mimicry, but their function in oral squamous cell carcinoma (OSCC) remains undefined. We employed a cohort of 82 cases of OSCC samples to examine the coexpression of Bcl-2 and Twist1 by immunohistochemistry and demonstrate the interaction between Bcl-2 and Twist1 by coimmunoprecipitation. Bcl-2 and Twist1 overexpression was associated with a poor pathological grade and tumor prognosis, and the two factors functions as a complex. Knocking down Bcl-2/Twist1 inhibited cell migration, decreased cell invasion and inversed cell epithelial-mesenchymal transition (EMT) procession. An animal model derived from the Tca8113 cell line was used to further validate the role of Bcl-2/Twist1 depletion in suppressing tumor EMT and growth. In conclusion, Bcl-2/Twist1 complex can be treated as a potential therapeutic target for OSCC.
Keywords: Bcl-2; EMT; Twist1; oral squamous cell carcinoma; tumor invasion.