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J. Biol. Chem., Vol. 281, Issue 43, 32217-32226, October 27, 2006

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Heparin Affin Regulatory Peptide/Pleiotrophin Mediates Fibroblast Growth Factor 2 Stimulatory Effects on Human Prostate Cancer Cells^*

Maria Hatziapostolou, Christos Polytarchou, Panagiotis Katsoris, Jose Courty^¶, and Evangelia Papadimitriou¹

From the Laboratory of Molecular Pharmacology, Department of Pharmacy, University of Patras, GR 26504 Patras, Greece, the Division of Genetics, Cell and Developmental Biology, Department of Biology, University of Patras, GR 26504 Patras, Greece, the ^¶Laboratoire de la Recherche sur la Croissance Cellulaire, la Reparation et la Regeneration Tissulaires, CNRS UMR 7149, Université Paris Val de Marne, Avenue du Général de Gaulle, 94010 Créteil, France

Fibroblast growth factor 2 (FGF2) is a pleiotropic growth factor that has been implicated in prostate cancer formation and progression. In the present study we found that exogenous FGF2 significantly increased human prostate cancer LNCaP cell proliferation and migration. Heparin affin regulatory peptide (HARP) or pleiotrophin seems to be an important mediator of FGF2 stimulatory effects, since the latter had no effect on stably transfected LNCaP cells that did not express HARP. Moreover, FGF2, through FGF receptors (FGFRs), significantly induced HARP expression and secretion by LNCaP cells and increased luciferase activity of a reporter gene vector carrying the full-length promoter of HARP gene. Using a combination of Western blot analyses, as well as genetic and pharmacological inhibitors, we found that activation of FGFR by FGF2 in LNCaP cells leads to NAD(P)H oxidase-dependent hydrogen peroxide production, phosphorylation of ERK1/2 and p38, activation of AP-1, increased expression and secretion of HARP, and, finally, increased cell proliferation and migration. These results establish the role and the mode of activity of FGF2 in LNCaP cells and support an interventional role of HARP in FGF2 effects, providing new insights on the interplay among growth factor pathways within prostate cancer cells.

Received for publication, July 26, 2006

^* This work was supported by the European Social Fund (ESF) Operational Program for Educational and Vocational Training II (EPEAEK II, IRAKLEITOS) and by grants from non-profit source the Association pour la Recherche sur le Cancer, ARC FRANCE no. 3242. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed. Tel.:/Fax: 30-2610-969336; E-mail: epapad{at}upatras.gr.

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