1. 17-beta-estradiol activates maxi-K channels through a non-genomic pathway in human breast cancer cells.
- Author
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Coiret G, Matifat F, Hague F, and Ouadid-Ahidouch H
- Subjects
- Cell Line, Tumor, Cell Proliferation drug effects, Electrophysiology, Genome, Human, Humans, Patch-Clamp Techniques, Potassium Channel Blockers pharmacology, Receptors, Estrogen metabolism, Breast Neoplasms metabolism, Breast Neoplasms pathology, Estradiol pharmacology, Potassium Channels metabolism
- Abstract
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.
- Published
- 2005
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