Activation of β-catenin signaling is critical for doxorubicin-induced epithelial-mesenchymal transition in BGC-823 gastric cancer cell line

The epithelial-mesenchymal transition (EMT) is a fundamental process governing morphogenesis in multicellular organisms and has recently been implicated in promoting carcinoma invasion and metastasis. Besides their therapeutic effects, accumulating evidences suggest that chemotherapeutic agents also induced EMT and enhanced the malignancy of treated cancer cells; however, the mechanism(s) still remains unclear. Here, we investigated the role of beta-catenin signaling in doxorubicin (Dox)-induced EMT in human gastric cancer cell line BGC-823. We found that the transient treatment of Dox induced EMT and enhanced the in vitro migration ability of cancer cells. We also found that beta-catenin signaling was activated upon Dox treatment. Inhibition of beta-catenin by indomethacin (Indo) or siRNA suppressed Dox-induced EMT and decreased cancer cell migration ability. Our results showed that beta-catenin signaling was critical to Dox-induced EMT. Indo and other beta-catenin inhibitors may have a potential implication in prevention of gastric cancer metastasis.