Carcinogenesis, Vol 18, 925-933, Copyright © 1997 by Oxford University Press
WL Wang, W Porter, R Burghardt and SH Safe
Treatment of estrogen receptor (ER)-negative MDA-MB-468 human breast cancer
cells with 10 nM 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced
formation of a nuclear aryl hydrocarbon (Ah) receptor complex as determined
by ligand-binding and gel electrophoretic mobility shift assays. TCDD also
induced CYP1A1-dependent activity in MDA-MB-468 cells, which represents the
first ER-negative Ah receptor-positive human breast cancer cell line that
has been identified. Treatment of this cell line with TCDD and related
compounds also caused a 50% inhibition of cell growth, which resembled the
growth inhibitory effects previously reported for epidermal growth factor
(EGF). However, EGF expression is minimal in this cell line and is not
induced by TCDD; moreover, EGF and TCDD induced a different pattern of
oncogene expression and apoptosis in MDA-MB-468 cells. In contrast, TCDD
caused a rapid and sustained induction of transforming growth factor alpha
(TGF alpha) gene expression and secreted protein (nearly 2-fold); moreover,
the growth-inhibitory effects of TCDD could be blocked by antibodies to the
EGF receptor. In a separate experiment, it was shown that TGF alpha also
inhibited growth of MDA-MB-468 cells. The results of this study indicate
that the mechanism of growth inhibition of MDA- MB-468 cells by TCDD is due
to induction of TGF alpha, which is a potent antimitogen in this cell
breast cancer line.
ARTICLES
Mechanism of inhibition of MDA-MB-468 breast cancer cell growth by 2,3,7,8-tetrachlorodibenzo-p-dioxin
Department of Veterinary Physiology, Texas A&M University, College Station 77843-4466, USA.
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