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Vitamin D and androgen regulation of prostatic growth
Author(s) -
Leman Eddy S.,
Arlotti Julie A.,
Dhir Rajiv,
Getzenberg Robert H.
Publication year - 2003
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.10605
Subject(s) - medicine , endocrinology , testosterone (patch) , endogeny , calcitriol receptor , prostate , androgen , vitamin d and neurology , prostate cancer , castration , dihydrotestosterone , hormone , biology , cancer
Abstract Vitamin D has been reported to inhibit the growth of prostate cancer cells and model systems. In this study, we examined the interaction between 1,25‐dihydroxyvitamin D 3 (1,25 D) in the presence or absence of endogenous testosterone on the growth and development of the adult rat prostate. Male Sprague–Dawley rats (165 days old) were either kept intact or castrated. Seven days after castration, the rats were treated with vehicle (control) or 1,25 D for 3 weeks and then sacrificed. Both ventral and dorsal lateral prostates were harvested; whole tissue lysates were collected and AR and VDR protein levels were analyzed by immunoblot analyses. Administration of 1,25 D in the intact animals decreased the prostatic size by 40%, compared to control animals, whereas 1,25 D did not influence the size of the prostate in castrated rats. 1,25 D administration in intact groups also increased both the AR and VDR protein levels by ∼twofold, whereas in castrated groups, 1,25 D only increased the AR protein level by 1.5–2.5‐fold. 1,25 D in the presence of endogenous testosterone inhibits prostatic growth, whereas 1,25 D in the absence of endogenous testosterone does not affect prostatic growth. The growth inhibitory activity of 1,25 D in the presence of testosterone may be mediated through the ligand activated AR and VDR pathways. These studies may reveal important information about the potential efficacy of 1,25 D as well as hormonal status in understanding the development of prostate diseases. J. Cell. Biochem. 90: 138–147, 2003. © 2003 Wiley‐Liss, Inc.