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This Article Accepted manuscript (PDF) All Versions of this Article: ERC-08-0084v1 15/4/841    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Zhu, M.-L. Articles by Kyprianou, N. Search for Related Content PubMed PubMed Citation Articles by Zhu, M.-L. Articles by Kyprianou, N.

M Zhu, Urology and Toxicology, University of Kentucky, Lexington, United States
N Kyprianou, Urology, University of Kentucky, Lexington, KY, United States

Correspondence: Natasha Kyprianou, Email: natasha{at}uky.edu

Abstract

Androgens promote growth and differentiation of prostate cells through ligand activation of the androgen receptor (AR). Sensitization of the androgenic response by multifunctional growth factor signaling pathways is one of the mechanisms via which AR contributes to the emergence of androgen independent prostate tumors. The ability of AR to cross-talk with key growth factor signaling events towards the regulation of cell cycle, apoptosis and differentiation outcomes in prostate cancer cells is established. In this paper, we review the functional interaction between AR and an array of growth factor signal transduction events (including EGF, epidermal growth factor; FGF, fibroblast growth factor; IGF-1, insulin-like growth factor-1; VEFG, vascular endothelial growth factor; TGF-β, transforming growth factor-β) in prostate tumors. The significance of this derailed cross-talk between androgens and key signaling networks in prostate cancer progression and its value as a therapeutic forum targeting androgen-independent metastatic prostate cancer is discussed.