Epithelial-mesenchymal transition in prostatic disease

被引：27
作者：
Broster, Seth A. [1 ,2 ,3 ,4 ]
Kyprianou, Natasha [1 ,2 ,3 ,4 ]
机构：
[1] Univ Kentucky, Coll Med, Dept Urol, Lexington, KY 40506 USA
[2] Univ Kentucky, Coll Med, Dept Mol Biochem, Lexington, KY USA
[3] Univ Kentucky, Coll Med, Dept Pathol, Lexington, KY USA
[4] Univ Kentucky, Coll Med, Dept Toxicol & Canc Biol, Lexington, KY USA
来源：
FUTURE ONCOLOGY | 2015年 / 11卷 / 23期
关键词：
benign growth; metastasis; prostate cancer; therapeutic response; tumor microenvironment; GROWTH-FACTOR-BETA; CIRCULATING TUMOR-CELLS; RAT VENTRAL PROSTATE; CANCER STEM-CELLS; ANDROGEN RECEPTOR; E-CADHERIN; MATRIX METALLOPROTEINASES; EXPRESSION; BENIGN; SUMOYLATION;
D O I：
10.2217/fon.15.253
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
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.
引用
收藏
页码：3197 / 3206
页数：10
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