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Department of Radiation Oncology, Long Island Jewish Medical Center, The Long Island Campus for the Albert Einstein College of Medicine, New Hyde Park, New York 11040 [S. F., Q. M., J. G., M. Y., I. D. G., E. M. R.], and Department of Pharmacology and Toxicology, Medical College of Virginia, Commonwealth University, Richmond, Virginia 23298 [B. G.]
Epidemiological studies suggest that moderate alcohol consumption
increases the risk of breast cancer, and that alcohol combined with
estrogen replacement therapy may synergistically enhance the risk.
However, the mechanism(s) of alcohol-induced mammary cancer is unknown.
In human breast cancer cell lines, we found that ethanol (EtOH) caused
a dose-dependent increase of up to 10- to 15-fold in the
transcriptional activity of the liganded estrogen receptor (ER-
),
but did not activate the nonliganded receptor. Significant
stimulation of ER- activity was observed at EtOH concentrations
comparable with or less than blood alcohol levels associated with
intoxication and at doses below the threshold for in
vitro cytotoxicity. These findings may be explained, in part,
by an EtOH-induced down-regulation of the expression of BRCA1, a
potent inhibitor of ER- activity, and, in part, by a modest increase
in the ER- levels. Our findings suggest that inactivation of
BRCA1 and increased estrogen-responsiveness might
contribute to alcohol-induced breast cancer.
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