Abstract
Epithelial–mesenchymal transition (EMT) has a crucial role during embryonic development and has also come under intense scrutiny as a mechanism through which esophageal squamous cell cancer (ESCC) progresses to become metastatic. Transforming growth factor beta (TGF-β)-mediated EMT has been observed in a variety of cell types and has been identified as the main inducer of EMT in many types of cancer. Akt activity is involved in TGF-β-mediated EMT; however, its precise relationship and role in EMT in ESCC has not been well explained to date. Our data demonstrated that in human ESCC tissues Akt and its activated form, phosphorylated-Akt (p-Akt), were overexpressed; in addition, Akt and p-Akt were negatively correlated with epithelial cadherin (E-cadherin). In EC-9706 cells, exogenous TGF-β1 could induce EMT and at the same time could increase the EC-9706 cell invasive and metastatic ability. Moreover, Akt knockdown by small-interfering RNA could attenuate the EMT induced by TGF-β1 by increasing the epithelial marker E-cadherin and decreasing the mesenchymal marker Vimentin. Silencing Akt expression could decrease the migration ability of EC-9706 cells efficiently. In short, Akt is likely to have a more important role in the EMT induced by TGF-β1 in EC-9706 and may contribute to the invasive and metastatic ability of EC-9706. Akt may be an effective therapeutic in advanced and metastatic ESCC.
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Acknowledgements
This work was supported by the National Natural Science Foundation of China [grant number 81071970] and the Medical Science and Technology Program of He’nan Province [grant number 200801006].
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Xuan, X., Zeng, Q., Li, Y. et al. Akt-mediated transforming growth factor-β1-induced epithelial–mesenchymal transition in cultured human esophageal squamous cancer cells. Cancer Gene Ther 21, 238–245 (2014). https://doi.org/10.1038/cgt.2014.23
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DOI: https://doi.org/10.1038/cgt.2014.23