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M200172200v1
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Papers In Press, published online ahead of print April 29, 2002
J. Biol. Chem, 10.1074/jbc.M200172200
Submitted on January 8, 2002
Revised on March 27, 2002
Accepted on April 26, 2002

Differential regulation of vascular endothelial growth factor expression by peroxisome proliferator-activated receptors in bladder cancer cells

Sylvie Fauconnet, Isabelle Lascombe, Eric Chabannes, Gerard- Louis Adessi, Beatrice Desvergne, Walter Wahli, and Hugues Bittard

IETG, Besancon 25000

Corresponding Author: echabannes{at}chu-besancon.fr

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 (PPAR gamma ) was involved in 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 MAP kinase kinase (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 for human bladder cancer in which excessive angiogenesis is a negative prognostic factor.


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