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Nucleic Acids Research 2005 33(20):6566-6578; doi:10.1093/nar/gki965
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Published online 24 November 2005

© The Author 2005. Published by Oxford University Press. All rights reserved
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions{at}oxfordjournals.org

Article

SIP1/ZEB2 induces EMT by repressing genes of different epithelial cell–cell junctions

Cindy Vandewalle, Joke Comijn, Bram De Craene, Petra Vermassen, Erik Bruyneel1, Henriette Andersen2, Eugene Tulchinsky3, Frans Van Roy4 and Geert Berx*

Unit of Molecular and Cellular Oncology, Department for Molecular Biomedical Research, VIB-Ghent University Belgium 1Laboratory of Experimental Cancerology, Department of Radiotherapy and Nuclear Medicine, Ghent University Belgium 2Department of Molecular Cancer Biology, Danish Cancer Society Denmark 3Department of Cancer Studies and Molecular Medicine, University of Leicester UK 4Molecular Cell Biology Unit, Department for Molecular Biomedical Research, VIB-Ghent University Belgium

*To whom correspondence should be addressed at Department for Molecular Biomedical Research, VIB-Ghent University, Technologiepark 927, 9052 Ghent (Zwijnaarde), Belgium. Tel: +32.0 9.3313740; Fax: +32.0 9.3313609; Email: geert.berx{at}dmbr.UGent.be

Received August 12, 2005. Revised November 2, 2005. Accepted November 2, 2005.

SIP1/ZEB2 is a member of the {delta}EF-1 family of two-handed zinc finger nuclear factors. The expression of these transcription factors is associated with epithelial mesenchymal transitions (EMT) during development. SIP1 is also expressed in some breast cancer cell lines and was detected in intestinal gastric carcinomas, where its expression is inversely correlated with that of E-cadherin. Here, we show that expression of SIP1 in human epithelial cells results in a clear morphological change from an epithelial to a mesenchymal phenotype. Induction of this epithelial dedifferentiation was accompanied by repression of several cell junctional proteins, with concomitant repression of their mRNA levels. Besides E-cadherin, other genes coding for crucial proteins of tight junctions, desmosomes and gap junctions were found to be transcriptionally regulated by the transcriptional repressor SIP1. Moreover, study of the promoter regions of selected genes by luciferase reporter assays and chromatin immunoprecipitation shows that repression is directly mediated by SIP1. These data indicate that, during epithelial dedifferentiation, SIP1 represses in a coordinated manner the transcription of genes coding for junctional proteins contributing to the dedifferentiated state; this repression occurs by a general mechanism mediated by Smad Interacting Protein 1 (SIP1)-binding sites.

The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors


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