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Published-Ahead-of-Print May 25, 2006, DOI:10.2164/jandrol.106.000554

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Androgens Induce Increases in Intracellular Calcium Via a G Protein-Coupled Receptor in LNcap Prostate Cancer Cells

Ying Hao Sun *, Xu Gao , Yuan Jie Tang , Chuan Liang Xu , and Lin Hui Wang

* To whom correspondence should be addressed. E-mail: gaoxu.changhai{at}gmail.com.

The receptor mechanism of testosterone-induced nongenomic Ca2+ signaling in prostate cancer cells is poorly understood. In this study, we investigated androgens-induced increases in intracellular Ca2+ in LNCaP human prostate cancer cells by using fura-2 as a Ca2+ probe. 5'-dihydrotestosterone (DHT) produced fast and transient increases in intracellular Ca2+ in LNCaP cells in a concentration-dependent manner. These effects were abolished by extracellular Ca2+ removal or pretreatment with L-type Ca2+ channel inhibitors (Nifedipine, Verapamil and Diltiazem). Pretreatment with endoplasmic reticulum ryanodine receptor blocker (procaine) or phospholipase C inhibitor (neomycin sulfate) did not alter the DHT induced Ca2+ influx. Ca2+ increases could also be induced by the impermeable testosterone conjugated to BSA. Neither antagonist of intracellular androgen receptors (CPA) nor protein synthesis inhibitor (cycloheximide) affects this fast Ca2+ influx. Furthermore, the effect of DHT was abolished in cells incubated with G protein inhibitors (pertussis toxin) and a nonhydrolyzable analog of GTP (GDP{beta}S), but not cells incubated with the tyrosine kinase inhibitor (genistein). The results indicate that androgens induced an L-type calcium channel dependent intracellular calcium increase in LNCaP prostate cancer cells. The rapid responses triggered by DHT did not appear to be mediated through classic intracellular androgen receptors or the c-Src kinase-AR complex or the sex hormone-binding globulin (SHBG). To our knowledge, we report for the first time that androgens induce calcium influx via a G protein-coupled receptor in LNCaP Prostate Cancer Cells. These results might provide a new explanation for progression of prostate cancer.


Key words: 5{alpha}-dihydrostestosterone • Ca2+ • prostate cancer cells • G Protein-Coupled Receptor






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Copyright © 2006 by The American Society of Andrology.