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Transforming growth factor-β1 induces epithelial-to-mesenchymal transition in human lung cancer cells via PI3K/Akt and MEK/Erk1/2 signaling pathways
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  • 作者:Xiao-Feng Chen (1) cxf229900@yahoo.com.cn
    Hui-Jun Zhang (12)
    Hai-Bing Wang (1)
    Jun Zhu (4)
    Wen-Yong Zhou (1)
    Hui Zhang (1)
    Ming-Chuan Zhao (1)
    Jin-Mei Su (3)
    Wen Gao (1)
    Lei Zhang (1)
    Ke Fei (2)
    Hong-Tao Zhang (5)
    He-Yong Wang (6) heyongwang@hotmail.com.cn
  • 关键词:TGF ; β1 – EMT – A549 – PI3K/Akt – MAPK/Erk1/2
  • 刊名:Molecular Biology Reports
  • 出版年:2012
  • 出版时间:April 2012
  • 年:2012
  • 卷:39
  • 期:4
  • 页码:3549-3556
  • 全文大小:491.1 KB
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  • 作者单位:1. Department of Thoracic Surgury, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China2. Department of Thoracic Surgury, Tenth People’s Hospital of Tongji University, Shanghai, China3. Department of Integrated Chinese Medicine and Western Medicine, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China4. Department of Thoracic Surgury, Forth People’s Hospital of Wuxi, Jiangsu, China5. Laboratory of Cancer Molecular Genetics, Medical College of Soochow University, Suzhou, China6. Central Laboratory, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China
  • 刊物类别:Biomedical and Life Sciences
  • 刊物主题:Life Sciences
    Animal Anatomy, Morphology and Histology
    Animal Biochemistry
  • 出版者:Springer Netherlands
  • ISSN:1573-4978
文摘
Metastasis of tumor cells is associated with epithelial-to-mesenchymal transition (EMT), which is a process whereby epithelial cells lose their polarity and acquire new features of mesenchyme. EMT has been reported to be induced by transforming growth factor-β1 (TGF-β1), but its mechanism remains elusive. In this study, we performed a study to investigate whether PI3K/Akt and MAPK/Erk1/2 signaling pathways involved in EMT in the human lung cancer A549 cells. The results showed that after treated with TGF-β1 for 48 h, A549 cells displayed more fibroblast-like shape, lost epithelial marker E-cadherin and increased mesenchymal markers Vimentin and Fibronectin. Moreover, TGF-β1-induced EMT after 48 h was accompanied by increased of cell migration and change of Akt and Erk1/2 phosphorylation. In addition, EMT was reversed by PI3K inhibitor LY294002 and MEK1/2 inhibitor U0126, which suggested that A549 cells under stimulation of TGF-β1 undergo a switch into mesenchymal cells and PI3K/Akt and MAPK/Erk1/2 signaling pathways serve to regulate TGF-β1-induced EMT of A549 cells.

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