期刊
FEBS LETTERS
卷 584, 期 22, 页码 4646-4654出版社
WILEY
DOI: 10.1016/j.febslet.2010.10.038
关键词
Epithelial-to-mesenchymal transition; Mesenchymal-to-epithelial transition; Snail; Transforming growth factor-beta; Glucocorticoid; Reactive oxygen species
资金
- Natural Science Foundation of China [30730023, 30721065, 30623003]
- National Basic Research Program of China [2007CB947900]
- Shanghai Science Committee [088014199]
Epithelial-to-mesenchymal transition (EMT) has been implicated in various physiological and pathological events. In this study, we found that the synthetic glucocorticoid dexamethasone (Dex) can inhibit transforming growth factor-beta1-induced EMT and cell migration. We also demonstrated that Dex inhibits EMT through a mechanism involving the suppression of ROS generation. Surprisingly, Dex alone induced mesenchymal-to-epithelial transition (MET). Dexamethasone treatment abolished Snail1 binding to the E-cadherin promoter, suggesting that suppression of Snail1 contributes to the above roles of Dex. Our findings demonstrate that Dex functions as both a suppressor of EMT and as an inducer of MET and therefore may be implicated in certain pathophysiological events. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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