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Inhibition of androgen induces autophagy in benign prostate epithelial cells
Author(s) -
Li Mengqiang,
Yang Xu,
Wang Huili,
Xu Enci,
Xi Zhijun
Publication year - 2014
Publication title -
international journal of urology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.172
H-Index - 67
eISSN - 1442-2042
pISSN - 0919-8172
DOI - 10.1111/iju.12210
Subject(s) - autophagy , hyperplasia , prostate , apoptosis , medicine , cancer research , androgen , prostate cancer , immunohistochemistry , endocrinology , biology , cancer , hormone , biochemistry
Objective 5‐α Reductase inhibitor can reduce the volume of benign prostatic hyperplasia by lowering benign prostatic hyperplasia level and consequently inducing epithelial cells apoptosis. The present study investigated whether autophagy and apoptosis of benign prostatic hyperplasia epithelial cells are influenced by low benign prostatic hyperplasia levels. Methods PWR ‐1 E prostate epithelial cells transfected with GFP ‐ LC 3 plasmid were subjected to androgen deprivation conditions. Then the autophagic puncta were evaluated by fluorescence microscopy, and the cellular apoptosis rate was detected by 4, 6‐diamidino‐2‐phenylindole staining after blocking of autophagic process by 3‐methyladenine. Furthermore, autophagy status was also determined in hyperplasia prostate tissues from 5‐α reductase inhibitor‐treated patients by immunohistochemistry. Results In the androgen deprivation medium, autophagic punta increased markedly in PWR ‐1 E cells, and blockage of autophagy by 3‐methyladenine significantly promoted PWR ‐1 E cells’ apoptosis rate. In vivo , the expression of LC 3 protein (an important autophagic marker) in hyperplasia prostate tissue significantly increased after 5‐α reductase inhibitor treatment. Meanwhile, the prostate‐specific antigen, as an inner control, decreased. Conclusion 5‐α Reductase inhibitor treatment increases autophagy and possibly decreases the apoptosis of prostate epithelial cells.

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