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

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• 作者：Rongfei Han (1)
  Jie Xiong (1)
  Ruijing Xiao (1)
  Ehtisham Altaf (1)
  Jin Wang (1)
  Yanping Liu (1)
  Hui Xu (1)
  Qianshan Ding (1)
  Qiuping Zhang (1)
  
• 关键词：EMT ; metastasis ; β ; catenin signaling ; indomethacin
• 刊名：Tumor Biology
• 出版年：2013
• 出版时间：February 2013
• 年：2013
• 卷：34
• 期：1
• 页码：277-284
• 全文大小：577KB
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• 作者单位：Rongfei Han (1)
  Jie Xiong (1)
  Ruijing Xiao (1)
  Ehtisham Altaf (1)
  Jin Wang (1)
  Yanping Liu (1)
  Hui Xu (1)
  Qianshan Ding (1)
  Qiuping Zhang (1)
  
  1. Department of Immunology, Wuhan University School of Basic Medical Science, Dong Hu Road 185, Wuchang, Wuhan, Hubei, 430071, People’s Republic of China
  
• ISSN：1423-0380

文摘

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 β-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 β-catenin signaling was activated upon Dox treatment. Inhibition of β-catenin by indomethacin (Indo) or siRNA suppressed Dox-induced EMT and decreased cancer cell migration ability. Our results showed that β-catenin signaling was critical to Dox-induced EMT. Indo and other β-catenin inhibitors may have a potential implication in prevention of gastric cancer metastasis.