17 beta-estradiol stimulates a rapid Ca2+ influx in LNCaP human prostate cancer cells.

Prostate growth is known to be controlled by steroids such as androgens and estradiol. For this reason steroids (estradiol, adrenal androgens) or steroid inhibitors are commonly used as palliative treatments for prostate carcinoma. In view of the pivotal role played by Ca2+ ions in cell proliferation, we decided to investigate the effects of 17 beta-estradiol (E2) on intracellular calcium concentration ([Ca2+]i) in a human prostate tumor cell line. LNCaP. In this study, we show that E2 induced a dose-dependent (0.1-100 nmol/l) influx of Ca2+ in these cells. These effects occurred rap dly after the beginning of the ejection and were maintained in the presence of the hormone (plateau phase). Estradiol-induced Ca2+ influx was unaffected by the saturation of the androgen receptor with pure antiandrogen flutamide. The use of tamoxifen, an antiestrogen binding to nuclear receptors, or E2 covalently linked to bovine serum albumin that cannot penetrate the cell membrane, did not block the ([Ca2+]i) response. Our results suggest the existence of E2 binding sites at the plasma membrane surface of LNCaP cells, linked to calcium signalling and, more specifically, Ca2+ channels.