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 NFκB 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.
Glycogen synthase kinase-3 is an endogenous inhibitor of Snail transcription
R. Bachelder,Sang-Oh Yoon,C. Francı́,A. G. de Herreros,A. Mercurio
Published 2005 in Journal of Cell Biology
ABSTRACT
PUBLICATION RECORD
- Publication year
2005
- Venue
Journal of Cell Biology
- Publication date
2005-01-03
- Fields of study
Biology, Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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