title: Epithelial-mesenchymal transition in prostatic disease.
abstract: A fully differentiated epithelium of the normal prostate gland allows epithelial cells to de-differentiate into mesenchymal-like derivatives via the process of epithelial-mesenchymal transition (EMT) and redifferentiate via the reverse process, mesenchymal-epithelial transition. This review discusses the phenotypic changes associated with EMT and its programming in the development of the two growth disorders of the aging prostate gland, benign prostatic hyperplasia and prostate adenocarcinoma. Considering the cellular heterogeneity that characterizes both conditions, identifying the transcriptional programming of the phenotypic framework defining EMT and its reverse process mesenchymal-epithelial transition in their pathological landscape will enable novel platforms for biomarker-driven therapeutics and their implementation in benign prostatic hyperplasia and prostate cancer.
authors.affiliation: Departments of Urology, Molecular Biochemistry, Pathology, Toxicology & Cancer Biology, University of Kentucky College of Medicine, Lexington, KY, USA.
authors.forename: Seth A
authors.initials: SA
authors.lastname: Broster
authors.affiliation: Departments of Urology, Molecular Biochemistry, Pathology, Toxicology & Cancer Biology, University of Kentucky College of Medicine, Lexington, KY, USA.
authors.forename: Natasha
authors.initials: N
authors.lastname: Kyprianou
mesh_terms: D000818:Animals; D060833:Cellular Microenvironment / Q000235:genetics; D044127:Epigenesis, Genetic; D058750:Epithelial-Mesenchymal Transition / Q000235:genetics; D005786:Gene Expression Regulation; D006801:Humans; D008297:Male; D010641:Phenotype; D011469:Prostatic Diseases / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D011470:Prostatic Hyperplasia / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D011471:Prostatic Neoplasms / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D015398:Signal Transduction; D058207:Sumoylation
keywords: benign growth; metastasis; prostate cancer; therapeutic response; tumor microenvironment