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The molecular mechanisms of prostate cancer are still poorly understood, despite the threat that prostate cancer poses to the health of men worldwide. As prostate tumors are initially dependent on androgens for growth and survival, androgen deprivation therapy is the firstline treatment for prostate cancer patients. However, a hormonal-refractory (androgen independent) state often develops afterwards, and principal treatment options are palliative because of the tumor progression, which is characterized by uncontrolled growth and metastasis associated with androgen independence. To date, no effective therapy can abrogate prostate cancer progression to advanced, invasive forms. Recent evidence suggests that acquisition of androgen-independence may be due to upregulation of growth factor receptor signaling pathways, principally the epidermal growth factor receptor (EGFR)/ErbB/human epidermal receptor (HER) family (Craft et al., 1999), making it an attractive target for therapeutic intervention. EGFR/ErbB/HER signaling in cancer has been extensively studied for decades, and there have been a number of excellent reviews on the roles of ErbB receptors in the initiation and progression of a wide variety of cancers, including prostate cancer (Laskin & Sandler, 2004; Ratan et al., 2003; Yarden & Sliwkowski, 2001). Thus, this review chapter will focus more narrowly on EGFR phosphorylation, signaling, and trafficking, and their specific roles in prostate cancer development and progression (tumor growth and metastasis) given the growing literature in this area. Better understanding of the precise roles of divergent EGFR signaling pathways and their phenotypic consequences in prostate cancer (and normal prostate) will enable the development of more effective and selective therapies for this urologic disease.

Epidermal Growth Factor Receptor (EGFR) Phosphorylation, Signaling and Trafficking in Prostate Cancer