Low-dose ethanol suppresses 17beta-estradiol activity in GH4C1 pituitary tumor cells.
The interaction of chronic alcohol consumption with estrogen has been recognized in various tissues; however, the potential mechanism has not been clearly defined. In this study, we made the following observations: (a) 0.01% (v/v) ethanol (corresponding to 1.7 mM) significantly elevated estrogen receptor alpha (ERalpha) protein content, stimulated activator protein-1 (AP-1)-dependent ERalpha transcriptional activities, and ultimately enhanced GH4C1 cells growth in vitro and (b) the same concentration of ethanol suppressed the stimulatory effects of 17beta-estradiol (E2; 10 nM) on both cell growth and cellular PRL accumulate through attenuation of ERalpha actions at both the estrogen response element and the AP-1 site. These observations raise the question as to what extent ethanol influences signal transduction pathways controlled by E2 in experimental medicine and biology.
Wang
Guoxin
G
State Key Laboratories for AgroBiotechnology, College of Biological Sciences, China Agricultural University, Haidian District Beijing 100193, People's Republic of China.
Chen
Dawei
D
Luo
Haoshu
H
Liu
Jiali
J
Ji
Xiaowen
X
Fan
Jingjing
J
Cui
Sheng
S
D000236:Adenoma / Q000378:metabolism; D000818:Animals; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D004958:Estradiol / Q000494:pharmacology*; D004965:Estrogen Antagonists / Q000494:pharmacology*; D047628:Estrogen Receptor alpha / Q000235:genetics / Q000378:metabolism; D000431:Ethanol / Q000494:pharmacology*; D010911:Pituitary Neoplasms / Q000378:metabolism*; D051381:Rats; D015398:Signal Transduction / Q000187:drug effects; D018808:Transcription Factor AP-1 / Q000378:metabolism; D014158:Transcription, Genetic / Q000187:drug effects
D004965:Estrogen Antagonists; D047628:Estrogen Receptor alpha; D018808:Transcription Factor AP-1; D000431:Ethanol; D004958:Estradiol