Epidermal growth factor receptor in prostate cancer

Epidermal growth factor receptor (EGFR), an oncogenic receptor tyrosine kinase, is over-expressed/overactive in a majority of tumors of epithelial origin including prostate cancer. Our understandings on EGFR have been primarily focused on its tyrosine kinase dependent functions in the plasma membrane, based on which therapeutic agents have been developed and used clinically. However, interfering with the tyrosine kinase activity of EGFR for prostate cancer treatment has not produced satisfactory outcomes. Besides the canonical mechanisms that mediate the tyrosine kinase dependent plasma membrane EGFR, studies have also revealed some non-canonical mechanisms that mediate the functions of non-plasma membrane localized EGFR and the tyrosine kinase independent functions of EGFR. This review summarizes the canonical and non-canonical mechanisms by which EGFR executes its oncogenic functions and discusses the therapeutic potentials possessed by the non-canonical mechanisms of EGFR function for prostate cancer management.