Overexpression of β-Catenin Induces Cisplatin Resistance in Oral Squamous Cell Carcinoma

• Main Authors: Long Li, Hai-Chao Liu, Cheng Wang, Xiqiang Liu, Feng-Chun Hu, Nan Xie, Lanhai Lü, Xiaohua Chen, Hong-Zhang Huang
• Format: Article
• Language: English
• Published: Hindawi Limited 2016-01-01
• Series: BioMed Research International
• Online Access: http://dx.doi.org/10.1155/2016/5378567
• ISSN: 2314-6133; 2314-6141

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-3β, 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.