Premium
17‐β‐Estradiol activates maxi‐K channels through a non‐genomic pathway in human breast cancer cells
Author(s) -
Coiret Guyllaume,
Matifat Fabrice,
Hague Frédéric,
Ouadid-Ahidouch Halima
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.02.085
Subject(s) - iberiotoxin , charybdotoxin , estrogen receptor , estrogen , cancer cell , breast cancer , chemistry , membrane potential , cell growth , microbiology and biotechnology , biology , potassium channel , cancer research , cancer , endocrinology , medicine , biochemistry
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.