Abstract
Simple SummaryAlthough epithelial-to-mesenchymal transition (EMT) is a well-known cellular process involved during normal embryogenesis and wound healing, it also has a dark side; it is a complex process that provides tumor cells with a more aggressive phenotype, facilitating tumor metastasis and even resistance to therapy. This review focuses on the key pathways of EMT in the pathogenesis of prostate cancer and the development of metastases and evasion of currently available treatments.Prostate cancer, the second most common malignancy in men, is characterized by high heterogeneity that poses several therapeutic challenges. Epithelial–mesenchymal transition (EMT) is a dynamic, reversible cellular process which is essential in normal embryonic morphogenesis and wound healing. However, the cellular changes that are induced by EMT suggest that it may also play a central role in tumor progression, invasion, metastasis, and resistance to current therapeutic options. These changes include enhanced motility and loss of cell–cell adhesion that form a more aggressive cellular phenotype. Moreover, the reverse process (MET) is a necessary element of the metastatic tumor process. It is highly probable that this cell plasticity reflects a hybrid state between epithelial and mesenchymal status. In this review, we describe the underlying key mechanisms of the EMT-induced phenotype modulation that contribute to prostate tumor aggressiveness and cancer therapy resistance, in an effort to provide a framework of this complex cellular process.
Highlights
Prostate cancer (PCa) is the second most frequently diagnosed male malignancy and the second leading cause of cancer mortality in men [1]
Cancers 2021, 13, 2795 the available pharmaceutical therapeutic approach of PCa is that PCa unavoidably 2doefv2e9lops resistance to androgen deprivation therapy (ADT) at some stage and progresses to castration-resistant PCa (CRPC), which is characterized by invasiveness and metastatic tospcraesatdratoiof nC-RrePsCistacenltlsP;Cthai(sCpRhPeCn)o,mwehnicohnisstcilhlarreapcrteersieznetds bthyeinmvaajsoivr ecnaeussseaonfdPmCeat-arsetlaattiecd sdpereaathd. oTfhCusR,PuCndceerllsst;anthdiisnpghtehneocmelelunloanr astnildl rmepolreecsuelnatrs mtheechmaanjiosrmcsauusnedeorflyPiCnag-rtheleatperdodceeastsh.oTf hmuest,ausntadteicrstdainssdeimnginthaetiocenllouflaPrCanadremmoaleincuslaarcmhaelclheanngiesmfosrubnedtteerrlyminagntahgeepmroecnetssof oPf Cmae.tastatic dissemination of PCa remains a challenge for better management of PCa
Overexpression of N-cadherin in PCa cells may further provoke epithelial–mesenchymal transition (EMT), invasion, and metastasis; expression of N-cadherin is increased after androgen deprivation, and its aberrant expression is involved in metastatic CRPC [62,63]
Summary
Prostate cancer (PCa) is the second most frequently diagnosed male malignancy and the second leading cause of cancer mortality in men [1]. For African American men, the incidence rates are higher when compared to White men; alarmingly, they have the highest chance of being diagnosed at a younger age (
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