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lüll Store-operated Ca2+ channels in prostate cancer epithelial cells: function, regulation, and role in carcinogenesis Vanden Abeele F; Shuba Y; Roudbaraki M; Lemonnier L; Vanoverberghe K; Mariot P; Skryma R; Prevarskaya NCell Calcium 2003[May]; 33 (5-6): 357-73Ca2+ homeostasis mechanisms, in which the Ca2+ entry pathways play a key role, are critically involved in both normal function and cancerous transformation of prostate epithelial cells. Here, using the lymph node carcinoma of the prostate (LNCaP) cell line as a major experimental model, we characterize prostate-specific store-operated Ca2+ channels (SOCs)--a primary Ca2+ entry pathway for non-excitable cells--for the first time. We show that prostate-specific SOCs share major store-dependent, kinetic, permeation, inwardly rectifying, and pharmacological (including dual, potentiation/inhibition concentration-dependent sensitivity to 2-APB) properties with "classical" Ca2+ release-activated Ca2+ channels (CRAC), but have a higher single channel conductance (3.2 and 12pS in Ca2+- and Na+-permeable modes, respectively). They are subject to feedback inhibition via Ca2+-dependent PKC, CaMK-II and CaM regulatory pathways and are functionally dependent on caveolae integrity. Caveolae also provide a scaffold for spatial co-localization of SOCs with volume-regulated anion channels (VRAC) and their Ca2+-mediated interaction. The TRPC1 and TRPV6 members of the transient receptor potential (TRP) channel family are the most likely molecular candidates for the formation of prostate-specific endogenous SOCs. Differentiation of LNCaP cells to an androgen-insensitive, apoptotic-resistant neuroendocrine phenotype downregulates SOC current. We conclude that prostate-specific SOCs are important determinants in the transition to androgen-independent prostate cancer.|Biomarkers[MESH]|Calcium Channels/genetics/*metabolism[MESH]|Calcium/*metabolism[MESH]|Electrophysiology[MESH]|Endoplasmic Reticulum/metabolism[MESH]|Epithelial Cells/*metabolism/pathology[MESH]|Humans[MESH]|Kinetics[MESH]|Male[MESH]|Oligonucleotides, Antisense/pharmacology[MESH]|Prostatic Neoplasms/*metabolism/pathology[MESH]|RNA, Messenger/drug effects[MESH]|TRPC Cation Channels[MESH]|TRPV Cation Channels[MESH]|Tumor Cells, Cultured[MESH] |