A major clinical problem with PC (prostate cancer) is the cell's ability to survive and proliferate upon androgen withdrawal. Indeed, deregulated cell differentiation and proliferation, together with the suppression of apoptosis, provides the condition for abnormal tissue growth. Here, we examine the differential role of TRP (transient receptor potential) channels in the control of Ca2+ homoeostasis and growth of PC cells.
Conference Article| January 22 2007
Differential role of TRP channels in prostate cancer
N. Prevarskaya 1
*Inserm, U-800, Equipe labellisée par la Ligue Nationale contre le cancer, Villeneuve d'Ascq F-59655, France
†USTL (Université des Sciences et Technologies de Lille), Villeneuve d'Ascq F-59655, France
1To whom correspondence should be addressed (email Natacha.Prevarskaya@univ-lille1.fr).
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N. Prevarskaya, M. Flourakis, G. Bidaux, S. Thebault, R. Skryma; Differential role of TRP channels in prostate cancer. Biochem Soc Trans 1 February 2007; 35 (1): 133–135. doi: https://doi.org/10.1042/BST0350133
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