Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/16166
Title: SIP1/ZEB2 induces EMT by repressing genes of different epithelial cell-cell junctions.
Authors: Vandewalle, C.
Comijn, J.
De Craene B.
Vermassen, P.
Bruyneel, E.
Andersen, H.
Tulchinsky, Eugene
Van Roy F.
Berx, G.
First Published: 24-Nov-2005
Publisher: Oxford University Press (OUP)
Citation: Nucleic Acids Research, 2005, 33 (20), pp. 6566-6578
Abstract: SIP1/ZEB2 is a member of the deltaEF-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.
DOI Link: 10.1093/nar/gki965
ISSN: 0305-1048
eISSN: 1362-4962
Links: http://hdl.handle.net/2381/16166
http://nar.oxfordjournals.org/content/33/20/6566
Type: Journal Article
Rights: 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@oxfordjournals.org
Appears in Collections:Published Articles, Dept. of Cancer Studies and Molecular Medicine

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