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Originally published In Press as doi:10.1074/jbc.M200172200 on April 29, 2002

J. Biol. Chem., Vol. 277, Issue 26, 23534-23543, June 28, 2002
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Differential Regulation of Vascular Endothelial Growth Factor Expression by Peroxisome Proliferator-activated Receptors in Bladder Cancer Cells*

Sylvie FauconnetDagger §, Isabelle LascombeDagger §, Eric Chabannes||, Gérard-Louis Adessi**, Béatrice Desvergne, Walter Wahli, and Hugues Bittard||Dagger Dagger

From the Dagger  Institut d'Etudes et de Transfert de Gènes Bâtiment INSERM, 240 route de Dole, the || Service d'Urologie et d'Andrologie, Hôpital St Jacques, 2 place St Jacques, and the ** Service d'Endocrinologie et Oncologie Moléculaires, Centre Hospitalier Universitaire Jean Minjoz, 25000 Besançon, France, and the  Institut de Biologie Animale, Université de Lausanne, CH-1015 Lausanne, Suisse

The growth of any solid tumor depends on angiogenesis. Vascular endothelial growth factor (VEGF) plays a prominent role in vesical tumor angiogenesis regulation. Previous studies have shown that the peroxisome proliferator-activated receptor gamma  (PPARgamma ) was involved in the angiogenesis process. Here, we report for the first time that in two different human bladder cancer cell lines, RT4 (derived from grade I tumor) and T24 (derived from grade III tumor), VEGF (mRNA and protein) is differentially up-regulated by the three PPAR isotypes. Its expression is increased by PPARalpha , beta , and gamma  in RT4 cells and only by PPARbeta in T24 cells via a transcriptional activation of the VEGF promoter through an indirect mechanism. This effect is potentiated by an RXR (retinoid-X-receptor), selective retinoid LG10068 providing support for a PPAR agonist-specific action on VEGF expression. While investigating the downstream signaling pathways involved in PPAR agonist-mediated up-regulation of VEGF, we found that only the MEK inhibitor PD98059 reduced PPAR ligand-induced expression of VEGF. These data contribute to a better understanding of the mechanisms by which PPARs regulate VEGF expression. They may lead to a new therapeutic approach to human bladder cancer in which excessive angiogenesis is a negative prognostic factor.

* This work was supported by grants from INSERM, the Programme Hospitalier de Recherche Clinique, the Ligues Nationale et Régionale Contre le Cancer, the Groupe de Recherche d'Urologie de Besançon, and the Swiss National Science Foundation.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.

§ These authors contributed equally to this work.

Dagger Dagger To whom correspondence should be addressed: Service d'Urologie et d'Andrologie, Hôpital St. Jacques, 25000 Besançon, France. Tel.: 00-33-3-81-21-91-70; Fax: 00-33-3-81-21-91-73; E-mail: urologie@chu-besancon.fr.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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