Abstract
Prostate development, benign hyperplasia and cancer involve androgen and growth factor signaling as well as stromal–epithelial interactions. We review how DNA methylation influences these and related processes in other organ systems such as how proliferation is restricted to specific cell populations during defined temporal windows, how androgens elicit their actions and how cells establish, maintain and remodel DNA methylation in a time and cell specific fashion. We also discuss mechanisms by which hormones and endocrine disrupting chemicals reprogram DNA methylation in the prostate and elsewhere and examine evidence for a reawakening of developmental epigenetic pathways as drivers of prostate cancer and benign prostate hyperplasia.
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The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
Financial & competing interests disclosure
This Work Was Supported By Grants From The National Institutes Of Health Dk099328, Dk096074 And Es001332. The Authors Have No Other Relevant Affiliations Or Financial Involvement With Any Organization Or Entity With A Financial Interest In Or Financial Conflict With The Subject Matter Or Materials Discussed In The Manuscript Apart From Those Disclosed.
No Writing Assistance Was Utilized In The Production Of This Manuscript.