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J Biol Chem, Vol. 275, Issue 15, 10943-10953, April 14, 2000

E-cadherin Is a WT1 Target Gene*

Seiyu HosonoDagger , Isabelle GrossDagger §, Milton A. EnglishDagger , Karen M. Hajra, Eric R. Fearon, and Jonathan D. LichtDagger ||**Dagger Dagger

From the Dagger  Derald H. Ruttenberg Cancer Center, || Department of Medicine, and ** Department of Biochemistry and Molecular Biology, Mount Sinai School of Medicine, New York, New York 10029 and the  Department of Internal Medicine, Division of Molecular Medicine & Genetics, University of Michigan Medical Center, Ann Arbor, Michigan 48109

The WT1 tumor suppressor gene encodes a transcription factor that can activate and repress gene expression. Transcriptional targets relevant for the growth suppression functions of WT1 are poorly understood. We found that mesenchymal NIH 3T3 fibroblasts stably expressing WT1 exhibit growth suppression and features of epithelial differentiation including up-regulation of E-cadherin mRNA. Acute expression of WT1 in NIH 3T3 fibroblasts after retroviral infection induced murine E-cadherin expression. In transient transfection experiments, the human and murine E-cadherin promoters were activated by co-expression of WT1. E-cadherin promoter activity was increased in cells overexpressing WT1 and was blocked by a dominant negative form of WT1. WT1 activated the murine E-cadherin promoter through a conserved GC-rich sequence similar to an EGR-1 binding site as well as through a CAAT box sequence. WT1 produced in vitro or derived from nuclear extracts bound to the WT1-response element within the murine E-cadherin promoter, but not the CAAT box. E-cadherin, a gene important in epithelial differentiation and neoplastic transformation, represents a downstream target gene that links the roles of the WT1 in differentiation and growth control.


* The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ Supported by the Association Pour La Recherche sur le Cancer.

Dagger Dagger Scholar of the Leukemia and Lymphoma Society. Supported by National Institutes of Health Grant CA 59998.

** To whom correspondence should be addressed: Derald H. Ruttenberg Cancer Center, Mount Sinai School of Medicine, Box 1130, One Gustave L. Levy Pl., New York, NY 10029. Tel.: 212-659-5487; Fax: 212-849-2523; E-mail: jonathan.licht@mssm.edu.


Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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