Melatonin downregulates TRPC6, impairing store-operated calcium entry in triple-negative breast cancer cells

Melatonin has been reported to induce effective reduction in growth and development a variety of tumors, including breast cancer. In triple-negative cancer (TNBC) cells, melatonin attenuates features, such as tumor apoptosis resistance, through number still poorly characterized mechanisms. One biological process that is important for TNBC cells store-operated Ca2+ entry (SOCE), which modulated by TRPC6 expression function. We wondered whether might intersect with this pathway part its anticancer activity. show melatonin, the nanomolar range, significantly MDA-MB-231 cell viability, proliferation, migration time- concentration-dependent manner, without having any effect on nontumoral epithelial MCF10A cells. Pretreatment different concentrations reduced SOCE altering release from intracellular stores. By contrast, was unaffected melatonin. MDA-MB-468 line, not only attenuated migration, SOCE, but also or function channel Orai1. The exogenous overcame silencing inhibition impaired inhibitory SOCE. These findings indicate downregulation be involved melatonin's effects influx maintenance hallmarks point toward novel antitumoral mechanism