17‐β‐Estradiol activates maxi‐K channels through a non‐genomic pathway in human breast cancer cells

We have investigated the acute effects of 17‐β‐estradiol (E 2 ) on K + channels in MCF‐7 breast epithelial cancer cells. E 2 induced a rapid and irreversible augmentation of the K + current for all membrane potentials superior to −25 mV. The effect of E 2 was sensitive to Iberiotoxin, Charybdotoxin and TEA and can be elicited in the presence of the anti‐estrogen ICI 182 780 or be mimicked by the membrane impermeant form E 2 /BSA. Furthermore, E 2 /BSA was able to stimulate cell proliferation in a maxi‐K inhibitors‐sensitive manner. Thus, these results permit us to identify the maxi‐K channel as the molecular target of E 2 that regulates cell proliferation independently of the estrogen receptor.