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J Biol Chem, Vol. 275, Issue 15, 10943-10953, April 14, 2000
From the 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.
E-cadherin Is a WT1 Target Gene*
,§,,
**
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 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.
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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