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Differential role of transient receptor potential channels in Ca2+ entry and proliferation of prostate cancer epithelial cells.: Role of TRP Channels in Proliferation

Abstract : One major clinical problem with prostate cancer is the cells' ability to survive and proliferate upon androgen withdrawal. Because Ca2+ is central to growth control, understanding the mechanisms of Ca2+ homeostasis involved in prostate cancer cell proliferation is imperative for new therapeutic strategies. Here, we show that agonist-mediated stimulation of alpha1-adrenergic receptors (alpha1-AR) promotes proliferation of the primary human prostate cancer epithelial (hPCE) cells by inducing store-independent Ca2+ entry and subsequent activation of nuclear factor of activated T cells (NFAT) transcription factor. Such an agonist-induced Ca2+ entry (ACE) relied mostly on transient receptor potential canonical 6 (TRPC6) channels, whose silencing by antisense hybrid depletion decreased both hPCE cell proliferation and ACE. In contrast, ACE and related growth arrest associated with purinergic receptors (P2Y-R) stimulation involved neither TRPC6 nor NFAT. Our findings show that alpha1-AR signaling requires the coupled activation of TRPC6 channels and NFAT to promote proliferation of hPCE cells and thereby suggest TRPC6 as a novel potential therapeutic target.
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https://www.hal.inserm.fr/inserm-00137697
Contributor : Matthieu Flourakis <>
Submitted on : Friday, September 4, 2009 - 2:08:49 PM
Last modification on : Thursday, February 13, 2020 - 3:06:03 PM
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Stephanie Thebault, Matthieu Flourakis, Karine Vanoverberghe, Franck Vandermoere, Morad Roudbaraki, et al.. Differential role of transient receptor potential channels in Ca2+ entry and proliferation of prostate cancer epithelial cells.: Role of TRP Channels in Proliferation. Cancer Research, American Association for Cancer Research, 2006, 66 (4), pp.2038-47. ⟨10.1158/0008-5472.CAN-05-0376⟩. ⟨inserm-00137697⟩

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