Glucocorticoid induces mesenchymal-to-epithelial transition and inhibits TGF-β1-induced epithelial-to-mesenchymal transition and cell migration

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cadherins / genetics
  • Cell Line
  • Cell Movement / drug effects*
  • Dexamethasone / pharmacology*
  • Epithelial Cells / cytology*
  • Epithelial-Mesenchymal Transition / drug effects*
  • Humans
  • Mesoderm / cytology*
  • Mesoderm / drug effects*
  • Mesoderm / metabolism
  • Mifepristone / pharmacology
  • Promoter Regions, Genetic
  • Reactive Oxygen Species / metabolism
  • Snail Family Transcription Factors
  • Transcription Factors / metabolism
  • Transforming Growth Factor beta1 / pharmacology*


  • Cadherins
  • Reactive Oxygen Species
  • SNAI1 protein, human
  • Snail Family Transcription Factors
  • Transcription Factors
  • Transforming Growth Factor beta1
  • Mifepristone
  • Dexamethasone