TAZ overexpression is associated with epithelial-mesenchymal transition in cisplatin-resistant gastric cancer cells

被引:23
作者
Ge, Liang [1 ]
Li, Dong-Song [2 ]
Chen, Fbi [3 ]
Feng, Ji-Dong [4 ]
Li, Bai [5 ]
Wang, Tie-Jun [6 ]
机构
[1] Jilin Univ, Hosp 1, Dept Anesthesiol, Changchun 130021, Jilin, Peoples R China
[2] Jilin Univ, Hosp 1, Dept Surg, Changchun 130021, Jilin, Peoples R China
[3] Jilin Prov Tumor Hosp, Abdominal Tumor Med Dept, Changchun 130021, Jilin, Peoples R China
[4] Jilin Prov Hosp Tradit Chinese Med, Dept Normal Surg, Changchun 130021, Jilin, Peoples R China
[5] Jilin Univ, Hosp 1, Dept Colorectal & Anal Surg, Changchun 130021, Jilin, Peoples R China
[6] Jilin Univ, Hosp 1, Dept Orthoped Traumatol, Changchun 130021, Jilin, Peoples R China
关键词
gastric cancer; chemoresistance; cisplatin; TAZ; epithelial-mesenchymal transition; DOWN-REGULATION; ANTITUMOR-ACTIVITY; HIPPO PATHWAY; ACQUISITION; SENSITIVITY; ACTIVATION; PHENOTYPE; YAP/TAZ; ADENOCARCINOMA; GEMCITABINE;
D O I
10.3892/ijo.2017.3998
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Gastric cancer is one of the common malignant diseases. The poor treatment outcome is mainly due to chemotherapeutic resistance. Therefore, it is important to determine the molecular mechanism of drug resistance in gastric cancer. To explore the mechanisms of cisplatin resistance in gastric cancer cells, several approaches were performed including MTT assay, real-time RT-PCR, western blot analysis, migration and invasion assays, wound healing assay, and transfection. We found that cisplatin-resistant (CR) gastric cancer cells acquired epithelial-mesenchymal transition (EMT) phenotype. The CR cells with EMT features obtained higher migratory and invasive activities. Moreover, we observed that TAZ was highly expressed in CR cells. Consistently, depletion of TAZ caused partial reversal of EMT to MET in CR cells. Our results suggest that TAZ plays a pivotal role in CR-induced EMT. Targeting TAZ could be a potential therapeutic strategy for gastric cancer.
引用
收藏
页码:307 / 315
页数:9
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