Since the discovery of TRP (Transient receptor Potential) and SOC (Store-Operated Channel) calcium channels, many labs have shown their involvement in the regulation of cell calcium homeostasis. In general, many alterations of these channels have been associated to syndromes, diseases and cancers. One of the mechanisms linking TRP and SOC alterations to the apparition of a pathology could be the perturbation of cell calcium homeostasis resulting from this alteration. Indeed, the involvement of these perturbations in carcinogenesis and cancer progression has been suggested by many teams. These perturbations could result from quantitative and functional variations affecting these channels or the proteins modulating their activity. Over the years, we have characterized the roles of SOC and TRPM8 channels in prostate cancer, and how different partner proteins can modulate their intracellular localization and their activity. We have also shown the interplay between both channels and their isoforms, and how they preside over prostate cancer cells fate.