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Abnormal expression of  β -catenin contributes to tumor development, progression, and metastasis in various cancers. However, little is known about the relationship between abnormal expression of  β -catenin and cisplatin chemotherapy in oral squamous cell carcinoma (OSCC). The present study aimed to investigate the effect of  β -catenin on OSCC cisplatin resistance and evaluated the drug susceptibility of stable cell lines with  β -catenin knockin and knockdown. In this study, we found that higher expression level of  β -catenin can be observed in CDDP-treated cell lines as compared with the control group. Furthermore, the expression levels of  β -catenin increased in both a concentration- and time-dependent manner with the cisplatin treatment. More importantly, the nuclear translocation of  β -catenin could also be observed by confocal microscope analysis. Stable cell lines with CTNNB1 knockin and knockdown were established to further investigate the potential role and mechanism of  β -catenin in the chemoresistance of OSCC in vitro and in vivo. Our findings indicated that overexpression of  β -catenin promoted cisplatin resistance in OSCC in vitro and in vivo. We confirmed that GSK-3 β , C-myc, Bcl-2, P-gp, and MRP-1 were involved in  β -catenin-mediated drug resistance. Our findings indicate that the Wnt/ β -catenin signaling pathway may play important roles in cisplatin resistance in OSCC.

Overexpression ofβ-Catenin Induces Cisplatin Resistance in Oral Squamous Cell Carcinoma