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Molecular and Cellular Biology, October 2006, p. 7561-7574, Vol. 26, No. 20
0270-7306/06/$08.00+0     doi:10.1128/MCB.00605-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Peroxisome Proliferator-Activated Receptor {gamma} Regulates E-Cadherin Expression and Inhibits Growth and Invasion of Prostate Cancer{ddagger}

Jean-Sébastien Annicotte,1 Irena Iankova,1,{dagger} Stéphanie Miard,1,{dagger} Vanessa Fritz,2 David Sarruf,1 Anna Abella,1 Marie-Laurence Berthe,3 Danièle Noël,2 Arnaud Pillon,1 François Iborra,3 Pierre Dubus,4 Thierry Maudelonde,3 Stéphane Culine,1 and Lluis Fajas1,3*

INSERM, U540, Equipe Avenir, Montpellier F-34090, France,1 INSERM, U475, Montpellier F-34090, France,2 Centre Hospitalier Universitaire Arnaud de Villeneuve, Laboratoire de Biologie Cellulaire, Montpellier F-34090, France,3 Université Victor Ségalen, EA2406 Histologie et Pathologie Moléculaire, Bordeaux F-33076, France4

Received 7 April 2006/ Returned for modification 10 May 2006/ Accepted 21 July 2006

Peroxisome proliferator-activated receptor {gamma} (PPAR{gamma}) might not be permissive to ligand activation in prostate cancer cells. Association of PPAR{gamma} with repressing factors or posttranslational modifications in PPAR{gamma} protein could explain the lack of effect of PPAR{gamma} ligands in a recent randomized clinical trial. Using cells and prostate cancer xenograft mouse models, we demonstrate in this study that a combination treatment using the PPAR{gamma} agonist pioglitazone and the histone deacetylase inhibitor valproic acid is more efficient at inhibiting prostate tumor growth than each individual therapy. We show that the combination treatment impairs the bone-invasive potential of prostate cancer cells in mice. In addition, we demonstrate that expression of E-cadherin, a protein involved in the control of cell migration and invasion, is highly up-regulated in the presence of valproic acid and pioglitazone. We show that E-cadherin expression responds only to the combination treatment and not to single PPAR{gamma} agonists, defining a new class of PPAR{gamma} target genes. These results open up new therapeutic perspectives in the treatment of prostate cancer.

* Corresponding author. Mailing address: Equipe Avenir, INSERM U540, 60 rue de Navacelles, F-34090 Montpellier, France. Phone: 0033 467 043 082. Fax: 0033 467 540 598. E-mail: fajas{at}montp.inserm.fr.

{ddagger} Supplemental material for this article may be found at http://mcb.asm.org/.

{dagger} These authors contributed equally to this work.

Molecular and Cellular Biology, October 2006, p. 7561-7574, Vol. 26, No. 20
0270-7306/06/$08.00+0     doi:10.1128/MCB.00605-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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