Abstract
Abstract Prostatic cancer is amongst the most common neoplasm in men. Inflammation and accelerated proliferation are important underlying causes for prostatic carcinogenesis. The role of estrogen in prostate physiology and pathophysiology has been growing rapidly. However some estrogen metabolites are more potent relative to parent estrogen. In the current work, the reciprocal role between inflammation and estrogen metabolism in prostatic microenvironment was investigated. Prostatitis was induced in normal and estrogen treated male rats by intraprostatic injection of 2% carragenan solution. After 48 h, animals were euthanized and prostate glands were collected. Prostatic inflammation and proliferation were confirmed by gross visual, histological and elevated TNF-α, PGE2 and cyclin-D1. Expression of estrogen metabolizing enzymes was assessed using real time PCR and estrogen metabolites within prostate tissue were assayed using LC-MS/MS. Inflammation combined with estrogen exposure showed exaggerated inflammatory and proliferative response. Estrogen metabolizing enzymes were over expressed in response to prostatic inflammation with sequential accumulation of catechol estrogens within prostatic tissues. Catechol estrogens were found to accelerate prostatic epithelial cell proliferation and alter their genetic stability. In conclusion, the current work provides experimental evidence that prostatic inflammation enhances estrogen metabolism to generate catechol estrogens within prostatic microenvironment. These may contribute in prostatic inflammation and accelerated proliferation and subsequently prostatic carcinogenesis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 543. doi:1538-7445.AM2012-543
Published Version
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