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

被引：34

作者：

Coiret, G ^{[1
]}

Matifat, F ^{[1
]}

Hague, F ^{[1
]}

Ouadid-Ahidouch, H ^{[1
]}

机构：

[1] Univ Picardie, Lab Physiol Cellulaire & Mol, Fac Sci, F-80039 Amiens, France

来源：

FEBS LETTERS | 2005年 / 579卷 / 14期

关键词：

maxi-K; estrogens; non-genomic effect; breast cancer; cell proliferation;

D O I：

10.1016/j.febslet.2005.02.085

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：2995 / 3000

页数：6

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