期刊
MOLECULAR BIOLOGY REPORTS
卷 39, 期 4, 页码 3549-3556出版社
SPRINGER
DOI: 10.1007/s11033-011-1128-0
关键词
TGF-beta 1; EMT; A549; PI3K/Akt; MAPK/Erk1/2
资金
- National Science Foundation of China [30872553, 30800631]
- Shanghai Science and Technology Committee [10JC1419200]
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-beta 1 (TGF-beta 1), 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-beta 1 for 48 h, A549 cells displayed more fibroblast-like shape, lost epithelial marker E-cadherin and increased mesenchymal markers Vimentin and Fibronectin. Moreover, TGF-beta 1-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-beta 1 undergo a switch into mesenchymal cells and PI3K/Akt and MAPK/Erk1/2 signaling pathways serve to regulate TGF-beta 1-induced EMT of A549 cells.
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