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Originally published In Press as doi:10.1074/jbc.M413878200 on January 11, 2005

J. Biol. Chem., Vol. 280, Issue 12, 11740-11748, March 25, 2005
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Wnt-dependent Regulation of the E-cadherin Repressor Snail*

Jong In Yook{ddagger}§, Xiao-Yan Li§, Ichiro Ota§, Eric R. Fearon§¶||**, and Stephen J. Weiss§**{ddagger}{ddagger}

From the {ddagger}Department of Oral Pathology, BK21 Project for Medical Science, College of Dentistry, Yonsei University, Seoul 120-742, Korea and the Division of Molecular Medicine & Genetics, Departments of §Internal Medicine, Human Genetics, and ||Pathology and the **University of Michigan Comprehensive Cancer Center, University of Michigan, Ann Arbor, Michigan 48109

Down-regulation of E-cadherin marks the initiation of the epithelial-mesenchymal transition, a process exploited by invasive cancer cells. The zinc finger transcription factor, Snail, functions as a potent repressor of E-cadherin expression that can, acting alone or in concert with the Wnt/{beta}-catenin/T cell factor axis, induce an epithelial-mesenchymal transition. Although mechanisms that coordinate signaling events initiated by Snail and Wnt remain undefined, we demonstrate that Snail displays {beta}-catenin-like canonical motifs that support its GSK3{beta}-dependent phosphorylation, {beta}-TrCP-directed ubiquitination, and proteasomal degradation. Accordingly, Wnt signaling inhibits Snail phosphorylation and consequently increases Snail protein levels and activity while driving an in vivo epithelial-mesenchymal transition that is suppressed following Snail knockdown. These findings define a potential mechanism whereby Wnt signaling stabilizes Snail and {beta}-catenin proteins in tandem fashion so as to cooperatively engage transcriptional programs that control an epithelial-mesenchymal transition.

Received for publication, December 9, 2004 , and in revised form, January 5, 2005.

* This work was supported by Medical Science and Engineering Research Program of the Korea Science & Engineering Foundation Grant R13-2003-013 (to J. I. Y.), National Institutes of Health Grants R01 CA071699 (to S. J. W.) and R01 CA088308 (to S. J. W.), Komen Foundation Grant BCTR00-000572 (to S. J. W.), and National Institutes of Health Grant R01 CA085463 (to E. R. F.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

{ddagger}{ddagger} To whom correspondence should be addressed: University of Michigan, 5403 Life Sciences Institute, 210 Washtenaw, Ann Arbor, MI 48109-2216. Tel.: 734-764-0030; Fax: 734-647-7950; E-mail: SJWEISS{at}umich.edu.


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