Abstract
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 CRcells with EMT features obtained higher migratory and invasive activities. Moreover, we observed that TAZ was highly expressed in CRcells. Consistently, depletion of TAZ caused partial reversal of EMT to MET in CRcells. Our results suggest that TAZ plays a pivotal role in CR-induced EMT. Targeting TAZ could be a potential therapeutic strategy for gastric cancer.
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