Casticin inhibits invasion and proliferation via downregulation of β-catenin and reversion of EMT in oral squamous cell carcinoma.

Background Casticin expresses multiple anti-cancer activities, whereas the effect of casticin on oral squamous cell carcinoma (OSCC) is still unclear. beta-catenin signaling plays a crucial role in the epithelial-mesenchymal transition which is closely related to tumorigenesis. Herein, we aimed to study the functions of casticin on invasion and migration of OSCC, and clarify whether the effect of casticin on OSCC has a relationship with beta-catenin signaling. Methods Human OSCC cell lines UM1 and HSC-3 were treated with different concentrations of casticin. The cell viability was evaluated by MTT and soft agar colony formation. Transwell assay and wound-healing assay were performed to measure the ability of cell invasion and migration. The protein expression was assessed by Western blotting. Results Casticin displayed inhibitory activities of cell viability, invasion, and migration on OSCC cell lines. Meanwhile, casticin could reverse EMT process and inhibit the expression of beta-catenin in OSCC. Knock-down or overexpression of beta-catenin could alter the effect of casticin on OSCC. Conclusions Casticin impaired invasion and migration of OSCC by inhibition of beta-catenin and reversal of EMT and could be a potential anti-cancer bioactive agent.