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BioMed Research International
Volume 2016 (2016), Article ID 5378567, 11 pages
http://dx.doi.org/10.1155/2016/5378567
Research Article

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

1Department of Oral and Maxillofacial Surgery, Guanghua School and Hospital of Stomatology, Sun Yat-sen University, Guangzhou 510055, China
2Guangdong Key Laboratory of Stomatology, Sun Yat-sen University, Guangzhou 510074, China
3Department of Oral Pathology, Guanghua School and Hospital of Stomatology, Sun Yat-sen University, Guangzhou 510055, China

Received 2 May 2016; Accepted 22 June 2016

Academic Editor: Antonello Merlino

Copyright © 2016 Long Li et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Abnormal expression of -catenin contributes to tumor development, progression, and metastasis in various cancers. However, little is known about the relationship between abnormal expression of -catenin and cisplatin chemotherapy in oral squamous cell carcinoma (OSCC). The present study aimed to investigate the effect of -catenin on OSCC cisplatin resistance and evaluated the drug susceptibility of stable cell lines with -catenin knockin and knockdown. In this study, we found that higher expression level of -catenin can be observed in CDDP-treated cell lines as compared with the control group. Furthermore, the expression levels of -catenin increased in both a concentration- and time-dependent manner with the cisplatin treatment. More importantly, the nuclear translocation of -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 -catenin in the chemoresistance of OSCC in vitro and in vivo. Our findings indicated that overexpression of -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 -catenin-mediated drug resistance. Our findings indicate that the Wnt/-catenin signaling pathway may play important roles in cisplatin resistance in OSCC.