Local growth hormone promotes benign prostatic hyperplasia.
Prostate cells expressing local growth hormone rise over 10-fold after age 60.
Local growth hormone promotes benign prostatic hyperplasia.
Locally produced nonpituitary growth hormone (npGH) promotes DNA damage accumulation and epithelial-mesenchymal transition (epithelial-mesenchymal transition) in aging human colon epithelium.
We hypothesized that local prostate GH action may promote epithelial-mesenchymal transition and contribute to benign prostatic hyperplasia pathogenesis.
GH receptor (GH receptor) and npGH are expressed in normal human prostate and benign prostatic hyperplasia (benign prostatic hyperplasia) prevalence increases with age.
GH-treated human primary prostate epithelial cells, normal prostate cells, and primary cell cultures derived from resected benign prostatic hyperplasia specimens exhibited enhanced DNA damage and activated epithelial-mesenchymal transition, with induced TWIST2 and suppressed E-cadherin, as well as increased Ki67, cell motility, and proliferation.
Prostate GH receptor signaling may be an attractive therapeutic target for benign prostatic hyperplasia.