Fiche publication
Date publication
décembre 2004
Auteurs
Membres identifiés du Cancéropôle Est :
Dr ETIQUE Nicolas
,
Pr FLAMENT Stéphane
,
Dr GRILLIER-VUISSOZ Isabelle
Tous les auteurs :
Etique N, Chardard D, Chesnel A, Flament S, Grillier-Vuissoz I
Lien Pubmed
Résumé
Alcohol consumption is known to be an increased risk factor for breast cancer, but the underlying molecular mechanisms are not well understood. We have recently shown that the exposure of MCF-7 breast cancer cells to 0.1% ethanol enhanced their proliferation and increased their content in both estrogen receptor-alpha (ERalpha) and aromatase. The aim of the present work was to determine if the effects of ethanol could be mimicked by other short-chain aliphatic alcohols such as methanol and 1-butanol. Our results show that these compounds do not stimulate MCF-7 cell proliferation. An increase in ERalpha content was observed by Western blot in methanol-treated cells, but this parameter was not affected in butanol-treated cells. Neither of these two alcohols induced an increase in aromatase mRNA level. So despite a similarity in molecular structure, these primary alcohols do not exert the same effects. Taken together, these results suggest that the increase in aromatase expression might be a key event required for the enhanced proliferation observed in the presence of ethanol.
Référence
Ann N Y Acad Sci. 2004 Dec;1030:78-85.
