17-beta-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 (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.
Coiret
Guyllaume
G
Laboratoire de Physiologie Cellulaire et Moléculaire, EA 2086, Université de Picardie Jules Verne, Faculté des Sciences, 33, Rue Saint-Leu 80039 Amiens, France.
Matifat
Fabrice
F
Hague
Frédéric
F
Ouadid-Ahidouch
Halima
H
D001943:Breast Neoplasms / Q000378:metabolism* / Q000473:pathology*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D004594:Electrophysiology; D004958:Estradiol / Q000494:pharmacology*; D015894:Genome, Human; D006801:Humans; D018408:Patch-Clamp Techniques; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000378:metabolism*; D011960:Receptors, Estrogen / Q000378:metabolism
D026902:Potassium Channel Blockers; D015221:Potassium Channels; D011960:Receptors, Estrogen; D004958:Estradiol