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17-beta-estradiol activates maxi-K channels through a non-genomic pathway in human breast cancer cells.

Authors:
Guyllaume Coiret Fabrice Matifat Frédéric Hague Halima Ouadid-Ahidouch

FEBS Lett 2005 Jun;579(14):2995-3000

Laboratoire de Physiologie Cellulaire et Moléculaire, EA 2086, Université de Picardie Jules Verne, Faculté des Sciences, 33, Rue Saint-Leu 80039 Amiens, France.

We have investigated the acute effects of 17-beta-estradiol (E2) on K+ channels in MCF-7 breast epithelial cancer cells. E2 induced a rapid and irreversible augmentation of the K+ current for all membrane potentials superior to -25 mV. The effect of E2 was sensitive to Iberiotoxin, Charybdotoxin and TEA and can be elicited in the presence of the anti-estrogen ICI 182780 or be mimicked by the membrane impermeant form E2/BSA. Furthermore, E2/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 E2 that regulates cell proliferation independently of the estrogen receptor.

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http://dx.doi.org/10.1016/j.febslet.2005.02.085DOI Listing
June 2005

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