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Originally published In Press as doi:10.1074/jbc.M108754200 on January 17, 2002

J. Biol. Chem., Vol. 277, Issue 13, 10824-10833, March 29, 2002
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Overexpression of an alpha 1H (Cav3.2) T-type Calcium Channel during Neuroendocrine Differentiation of Human Prostate Cancer Cells*

Pascal MariotDagger §, Karine VanoverbergheDagger , Nathalie Lalevée, Michel F. Rossier||, and Natalia PrevarskayaDagger

From the Dagger  Laboratoire de Physiologie Cellulaire, INSERM EPI9938, Bâtiment SN3, Université des Sciences et Technologies de Lille, 59655 Villeneuve d'Ascq Cédex, France and the  Division of Endocrinology & Diabetology, Department of Internal Medicine, || Laboratory of Clinical Chemistry, Department of Pathology, University Hospital, CH-1211 Geneva 14, Switzerland

Neuroendocrine differentiation of prostate epithelial cells is usually associated with an increased aggressivity and invasiveness of prostate tumors and a poor prognosis. However, the molecular mechanisms involved in this process remain poorly understood. We have investigated the possible expression of voltage-gated calcium channels in human prostate cancer epithelial LNCaP cells and their modulation during neuroendocrine differentiation. A small proportion of undifferentiated LNCaP cells displayed a voltage-dependent calcium current. This proportion and the calcium current density were significantly increased during neuroendocrine differentiation induced by long-term treatments with cyclic AMP permeant analogs or with a steroid-reduced culture medium. Biophysical and pharmacological properties of this calcium current suggest that it is carried by low-voltage activated T-type calcium channels. Reverse transcriptase-PCR experiments demonstrated that only a single type of LVA calcium channel mRNA, an alpha 1H calcium channel mRNA, is expressed in LNCaP cells. Quantitative real-time reverse transcriptase-PCR revealed that alpha 1H mRNA was overexpressed during neuroendocrine differentiation. Finally, we show that this calcium channel promotes basal calcium entry at resting membrane potential and may facilitate neurite lengthening. This voltage-dependent calcium channel could be involved in the stimulation of mitogenic factor secretion and could therefore be a target for future therapeutic strategies.

* This work was supported by the INSERM, Ligue Nationale contre le Cancer, Association pour la Recherche contre le Cancer, Fondation pour la Recherche Médicale, and Swiss National Science Foundation Grant 32-58948.99 (to M. F. R. and N. L.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ To whom correspondence should be addressed: Laboratoire de Physiologie Cellulaire, INSERM EPI9938, Bâtiment SN3, Université des Sciences et Technologies de Lille, 59655 Villeneuve d'Ascq Cédex, France. Tel.: 33-3-20-43-40-77; Fax: 33-3-20-43-40-66; E-mail: Pascal.Mariot@univ-lille1.fr.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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