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Published 3 January 2005. doi:10.1083/jcb.200409067
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 168, Number 1, 29-33
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Glycogen synthase kinase-3 is an endogenous inhibitor of Snail transcription

: implications for the epithelial–mesenchymal transition



Robin E. Bachelder1, Sang-Oh Yoon1, Clara Franci2, Antonio García de Herreros2, and Arthur M. Mercurio1

1 Department of Pathology, Division of Cancer Biology and Angiogenesis, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215
2 Unitat de Biologia Cellular i Molecular, Institut Municipal d'Investigació Mèdica, Universitat Pompeu Fabra, 08003 Barcelona, Spain

Correspondence to Robin E. Bachelder: rbacheld{at}bidmc.harvard.edu


Abstract

We report that the activity of glycogen synthase kinase-3 (GSK-3) is necessary for the maintenance of the epithelial architecture. Pharmacological inhibition of its activity or reducing its expression using small interfering RNAs in normal breast and skin epithelial cells results in a reduction of E-cadherin expression and a more mesenchymal morphology, both of which are features associated with an epithelial–mesenchymal transition (EMT). Importantly, GSK-3 inhibition also stimulates the transcription of Snail, a repressor of E-cadherin and an inducer of the EMT. We identify NF{kappa}B as a transcription factor inhibited by GSK-3 in epithelial cells that is relevant for Snail expression. These findings indicate that epithelial cells must sustain activation of a specific kinase to impede a mesenchymal transition.

Abbreviations used in this paper: EMT, epithelial–mesenchymal transition; GSK-3, glycogen synthase kinase-3; siRNA, small interfering RNA.


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