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17β-Estradiolid C^a influx rapid Ca2+ prostate cancer cells

Audy MC, Vacher P, Dufy B, 17β-Estradiol stimulates a rapid Ca²⁺ influx in LNCaP human prostate cancer cells. Eur J Endocrinol 1996;135:367–73. ISSN 0804–4643

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 17β-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 rapidly 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.

MC Audy, Laboratoire de Neurophysiologie, URA 1200, 146 rue Léo Saignat, Université de Bordeaux II, 33076 Bordeaux Cedex, France