Abstract
Numerous studies on the molecular basis of prostate cancer focus on the role of androgens, but estrogens have been shown to be linked to prostate cancer development and progression. In the present article, we reviewed the laboratory and clinical evidence, demonstrating that estrogens can be the cause of the development and progression of prostatic hyperplasia and prostate cancer. We also studied the more significant mechanisms related to estrogen action, which include: direct genotoxicity, hyperprolactinemia, inflammation, and receptor-mediated action. In addition, we analyzed the functions of the known estrogen receptors (alpha and beta) in diseases of the prostate. The evidence observed suggests that estrogen receptor alpha plays an essential role in the development of both the normal prostate and the cancer, whereas estrogen receptor beta is related to the differentiation of the prostatic epithelial tissue and numerous antiproliferative actions in prostate cancer. Nevertheless, some of their isoforms are associated with mechanisms of cancer initiation and progression. Finally, we believe that more studies related to estrogen action should be carried out to better understand the role estrogens play in the development of prostate cancer.
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