The prostate gland requires androgenic steroids for its appropriate embryological formation and postpubertal growth and, once at adult size, remains dependent on a continuous supply of androgens for its vitality and function. A reduction of the levels of circulating androgens will rapidly induce apoptosis of the cells of the prostate, leading to extensive glandular regression. Studies of rodent models of prostate response to castration have shown that there are some remarkable changes in the gene activity of prostate epithelial cells leading up to apoptosis. There is now evidence for a critical cell signaling pathway, regulated by c-fos expression, necessary for castration-induced apoptosis, as well as evidence that this signaling initiates an abrupt and transient alteration in the synthesis of fas antigen, p53, bax and bcl-2 proteins in the androgen receptor-expressing prostate epithelial cells, the cellular compartment that appears to be the most affected by castration. However, more recent studies suggest that these castration-induced effects on the prostate epithelial cells might be, at least in part, an indirect response to a critical reduction in blood flow to the prostate gland that precedes the onset of epithelial celt apoptosis. The castration effects on blood flow to the prostate gland seem to be related to vascular degeneration associated with apoptosis of a subset of prostate endothelial cells.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism