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J. Biol. Chem., Vol. 278, Issue 14, 11802-11810, April 4, 2003
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From The Burnham Institute, La Jolla Cancer Research Center, La
Jolla, California 92037, the § Sidney Kimmel Cancer
Center, San Diego, California 92121, the Cancer Center, Universtiy of
California at San Diego, La Jolla, California 92093, and the
¶ Istituto di Ricovero e Cura a Carattere Scientifico,
Neuromed, Pozzilli 86077, Italy
In the majority of aggressive tumorigenic
prostate cancer cells, the transcription factor Egr1 is overexpressed.
We provide new insights of Egr1 involvement in proliferation and
survival of TRAMP C2 prostate cancer cells by the identification
of several new target genes controlling growth, cell cycle progression,
and apoptosis such as cyclin D2, P19ink4d, and Fas. Egr1 regulation of
these genes, identified by Affymetrix microarray, was confirmed by
real-time PCR, immunoblot, and chromatin immunoprecipitation assays.
Furthermore we also showed that Egr1 is responsible for cyclin D2
overexpression in tumorigenic DU145 human prostate cells. The
regulation of these genes by Egr1 was demonstrated using Egr1 antisense
oligonucleotides that further implicated Egr1 in resistance to
apoptotic signals. One mechanism was illustrated by the ability of Egr1
to inhibit CD95 (Fas/Apo) expression, leading to insensitivity to FasL.
The results provide a mechanistic basis for the oncogenic role of Egr1
in TRAMP C2 prostate cancer cells.
Egr1 Promotes Growth and Survival of Prostate Cancer Cells
IDENTIFICATION OF NOVEL Egr1 TARGET GENES*
,, and
*
This work was supported by United States Public Health
Service Grants CA 67888 (to E. D. A.) and CA 84998, CA 76173, and CA84107 (all to D. M.); the California Cancer Research
Program (to D. M.); Department of Defense Grant DOD17-01-1-0005
(to E. D. A.); the Phillippe Foundation (to T. V. and V. B.); the Institut National de la Santé et de la
Recherche Médicale (to T. V.); and the Deutscher
Akademischer Austauschdienst (to A. K.-H.).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.
To whom correspondence may be addressed: Biologie et
Physiopathologie de la Peau, INSERM, Faculté de Médecine de
Nice, av de Valombrose, Nice 06107, France. Tel.: 33-4-93-37-76-48;
Fax: 33-4-93-81-14-04; E-mail: virolle@unice.fr (for T. V.) or The Burnham Inst., La Jolla, CA 92037. Tel.: 858-646-3137; E-mail: eadamson@burnham.org (for E. D. A.).
Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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