Yaxin Xie1, Liang Zhong1, Dingyu Duan1,2, Taiwen Li1. 1. State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Chinese Academy of Medical Sciences Research Unit of Oral Carcinogenesis and Management, West China Hospital of Stomatology, Sichuan University, Chengdu, China. 2. Department of Periodontology, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Abstract
BACKGROUND: Casticin expresses multiple anti-cancer activities, whereas the effect of casticin on oral squamous cell carcinoma (OSCC) is still unclear. β-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 β-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 β-catenin in OSCC. Knock-down or overexpression of β-catenin could alter the effect of casticin on OSCC. CONCLUSIONS: Casticin impaired invasion and migration of OSCC by inhibition of β-catenin and reversal of EMT and could be a potential anti-cancer bioactive agent.
BACKGROUND:Casticin expresses multiple anti-cancer activities, whereas the effect of casticin on oral squamous cell carcinoma (OSCC) is still unclear. β-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 β-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 β-catenin in OSCC. Knock-down or overexpression of β-catenin could alter the effect of casticin on OSCC. CONCLUSIONS:Casticin impaired invasion and migration of OSCC by inhibition of β-catenin and reversal of EMT and could be a potential anti-cancer bioactive agent.