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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.

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