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lüll TRPV6 channel controls prostate cancer cell proliferation via Ca(2+)/NFAT-dependent pathways Lehen'kyi V; Flourakis M; Skryma R; Prevarskaya NOncogene 2007[Nov]; 26 (52): 7380-5The transient receptor potential channel, subfamily V, member 6 (TRPV6), is strongly expressed in advanced prostate cancer and significantly correlates with the Gleason >7 grading, being undetectable in healthy and benign prostate tissues. However, the role of TRPV6 as a highly Ca(2+)-selective channel in prostate carcinogenesis remains poorly understood. Here, we report that TRPV6 is directly involved in the control of prostate cancer cell (LNCaP cell line) proliferation by decreasing: (i) proliferation rate; (ii) cell accumulation in the S-phase of cell cycle and (iii) proliferating cell nuclear antigen (PCNA) expression. We demonstrate that the Ca(2+) uptake into LNCaP cells is mediated by TRPV6, with the subsequent downstream activation of the nuclear factor of activated T-cell transcription factor (NFAT). TRPV6-mediated Ca(2+) entry is also involved in apoptosis resistance of LNCaP cells. Our results suggest that TRPV6 expression in LNCaP cells is regulated by androgen receptor, however, in a ligand-independent manner. We conclude that the upregulation of TRPV6 Ca(2+) channel in prostate cancer cells may represent a mechanism for maintaining a higher proliferation rate, increasing cell survival and apoptosis resistance as well.|*Cell Proliferation[MESH]|Apoptosis[MESH]|Calcium Channels/genetics/*metabolism[MESH]|Calcium Signaling[MESH]|Calcium/*metabolism[MESH]|Enzyme Inhibitors/pharmacology[MESH]|Humans[MESH]|Male[MESH]|NFATC Transcription Factors/*metabolism[MESH]|Prostatic Neoplasms/genetics/*metabolism[MESH]|S Phase/physiology[MESH]|Signal Transduction[MESH]|TRPV Cation Channels/genetics/*metabolism[MESH]|Thapsigargin/pharmacology[MESH]|Tumor Cells, Cultured[MESH] |