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-beta-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. (c) 2005 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.