Prostate cancer is a common and deadly
cancer among men. The heterogeneity that characterizes prostate
tumors contributes to clinical challenges in the diagnosis, prognosis, and treatment of this
malignancy. While localized
prostate cancer can be treated with surgery or
radiotherapy, metastatic disease to the lymph nodes and the bone requires aggressive treatment with
androgen deprivation treatment (ADT). Unfortunately, this often eventually progresses to metastatic
castration-resistant
prostate cancer (mCRPC). Advanced
prostate cancer treatment today involves 1st- and 2nd-line
taxane chemotherapy and 2nd-generation
antiandrogens. The process of epithelial mesenchymal transition (EMT), during which epithelial cells lose their adhesions and their polarity, is a critical contributor to
prostate cancer metastasis. In this article, we aim to integrate the current understanding of mechanisms dictating the dynamics of phenotypic EMT, with apoptosis outcomes in prostate
tumors in response to
antiandrogen and
taxane chemotherapy for the treatment of advanced disease. Novel insights into the signaling mechanisms that target the functional interface between apoptosis and EMT will be considered in the context of potential
clinical markers of
tumor prognosis, as well as for effective therapeutic targeting of α- and β-
adrenergic signaling (by novel and existing chemotherapeutic agents and
antiandrogens). Interfering with EMT and apoptosis simultaneously toward eradicating the
tumor mass is of major significance in combating the lethal disease and increasing patient survival.