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This Article Full Text Full Text (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 Google Scholar Articles by Zhu, M.-L. Articles by Kyprianou, N. PubMed PubMed Citation Articles by Zhu, M.-L. Articles by Kyprianou, N.

Departments of Urology and Toxicology, University of Kentucky College of Medicine, University of Kentucky Medical Center, Combs Research Building Room 306, Lexington, Kentucky 40536, USA

(Correspondence should be addressed to N Kyprianou; Email: nkypr2{at}uky.edu)

Androgens promote the 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 toward 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 epidermal growth factor; fibroblast growth factor; IGF1; vascular endothelial growth factor; 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.