title: Epithelial-to-mesenchymal transition in prostate cancer: paradigm or puzzle?
abstract: The lethal consequences of prostate cancer are related to its metastasis to other organ sites. Epithelial-to-mesenchymal transition (EMT) has received considerable attention as a conceptual paradigm to explain invasive and metastatic behavior during cancer progression. EMT is a normal physiologic process by which cells of epithelial origin convert into cells bearing mesenchymal characteristics. It has been proposed that EMT is co-opted by cancer cells during their metastatic dissemination from a primary organ to secondary sites, but the extent to which this recapitulates physiologic EMT remains uncertain. However, there is ample evidence that EMT-like states occur in, and may contribute to, prostate cancer progression and metastasis, and so has become a very active area of research. Here we review this evidence and explore recent studies that have aimed to better define the role and mechanisms of EMT in prostate cancer. While definitive evidence of something akin to physiologic EMT is still lacking in human prostate cancer, this area of research has nonetheless provided new avenues of investigation into the longstanding puzzles of metastasis, therapeutic resistance, and prognostic biomarkers.
authors.affiliation: Department of Molecular Physiology, Medical Scientist Training Program, Roy J. and Lucille A. Carver College of Medicine and Holden Comprehensive Cancer Center, The University of Iowa, Bowen Science Building, 51 Newton Road, Iowa City, IA 52242, USA.
authors.forename: Jones T
authors.initials: JT
authors.lastname: Nauseef
authors.forename: Michael D
authors.initials: MD
authors.lastname: Henry
mesh_terms: D000818:Animals; D002454:Cell Differentiation / Q000502:physiology; D018450:Disease Progression; D004847:Epithelial Cells / Q000473:pathology*; D058750:Epithelial-Mesenchymal Transition / Q000502:physiology*; D006801:Humans; D008297:Male; D059630:Mesenchymal Stem Cells / Q000473:pathology*; D009361:Neoplasm Invasiveness / Q000473:pathology; D011471:Prostatic Neoplasms / Q000209:etiology / Q000473:pathology*