Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences. 320 Yue-Yang Road, Shanghai 200031, China.
FEBS Lett. 2010 Nov 19;584(22):4646-54. doi: 10.1016/j.febslet.2010.10.038. Epub 2010 Oct 26.
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.
上皮-间充质转化（EMT）参与了各种生理和病理事件。在这项研究中，我们发现合成糖皮质激素地塞米松（Dex）可以抑制转化生长因子-β1 诱导的 EMT 和细胞迁移。我们还表明，Dex 通过抑制 ROS 生成的机制抑制 EMT。令人惊讶的是，Dex 本身诱导间充质-上皮转化（MET）。地塞米松处理消除了 Snail1 与 E-钙黏蛋白启动子的结合，表明抑制 Snail1 有助于 Dex 的上述作用。我们的研究结果表明，Dex 既可以作为 EMT 的抑制剂，也可以作为 MET 的诱导剂，因此可能与某些病理生理事件有关。
