Abstract
Prostate cancer (PC) remains a widespread malignancy in men. Since the androgen/androgen receptor (AR) axis is associated with the pathogenesis of prostate cancer, suppression of AR-dependent signaling by androgen deprivation therapy (ADT) still represents the primary intervention for this disease. Despite the initial response, prostate cancer frequently develops resistance to ADT and progresses. As such, the disease becomes metastatic and few therapeutic options are available at this stage. Although the majority of studies are focused on the role of AR signaling, compelling evidence has shown that estrogens and their receptors control prostate cancer initiation and progression through a still debated mechanism. Epithelial versus mesenchymal transition (EMT) is involved in metastatic spread as well as drug-resistance of human cancers, and many studies on the role of this process in prostate cancer progression have been reported. We discuss here the findings on the role of estrogen/estrogen receptor (ER) axis in epithelial versus mesenchymal transition of prostate cancer cells. The pending questions concerning this issue are presented, together with the impact of the available data in clinical management of prostate cancer patients.
Highlights
Despite diagnostic, clinical and therapeutic efforts, prostate cancer (PC) still represents a major urological disease associated with a significant morbidity
We present here the findings so far obtained on the molecular events underlying the Epithelial Mesenchymal Transition (EMT) controlled by the estrogen/estrogen receptors (ERs) axis in different models of prostate tissues and Prostate Cancer (PC)
The role of ERα has been further corroborated by recent findings showing that estrogen activation of ERα drives the expression of neurogenic locus notch homolog protein 1 (NOTCH1), thereby enhancing stemness and the EMT phenotype in a PC mouse model
Summary
Clinical and therapeutic efforts, prostate cancer (PC) still represents a major urological disease associated with a significant morbidity. Subsequent findings showed that BPH is driven by activation of an EMT program, accompanied by both the loss of E-cadherin and the increase of vimentin in epithelial cells from BPH specimens. It was demonstrated by the same group that the ERα-specific agonist, PPT promotes the expression of EMT markers in benign epithelial BPH-1 and RWPE-1 cell lines, cultured in both 2D and 3D models.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
