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[Cancer Research 55, 3902-3907, September 1, 1995]
© 1995 American Association for Cancer Research
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Estrogen Promotes Chemotherapeutic Drug Resistance by a Mechanism Involving Bcl-2 Proto-Oncogene Expression in Human Breast Cancer Cells1

Christine Teixeira, John C. Reed and M. A. Christine Pratt2

Department of Pharmacology, University of Ottawa, Ottawa, Ontario, Canada K1H 8M5 [C. T., M. A. C. P.] and La Jolla Cancer Research Foundation, Cancer Research Center, La Jolla, California 92037 [J. C. R.]

Recent studies have shown that the Bcl-2 protein suppresses programmed cell death or apoptosis induced by a variety of stimuli including chemotherapeutic drugs. Because estrogen promotes the survival of estrogen-dependent breast cancer cells in vivo, we investigated whether estrogen might regulate levels of Bcl-2 gene expression in an estrogen-responsive human breast cancer cell line. Estrogen receptor-positive MCF-7 human breast cancer cells cultured in the presence of estrogen express the 8.5-kb Bcl-2 mRNA transcript. Depletion of estrogen from the medium results in loss of expression of the mRNA, whereas reexposure to estrogen markedly induces the Bcl-2 transcript. The changes in Bcl-2 mRNA are paralleled by changes in Bcl-2 protein levels. Estrogen-induced increases in Bcl-2 are significantly inhibited by inclusion of the pure antiestrogen ICI 164,384 in the medium. The Bax protein that heterodimerizes with Bcl-2 and promotes cell death is expressed in MCF-7 cells grown in the presence of estrogen and is unaffected by culture in estrogen-free medium. Estrogen depletion doubles the sensitivity of MCF-7 cells to the cytotoxic effects of Adriamycin compared with cells cultured in medium supplemented with estrogen, consistent with a decrease in the Bcl-2 levels. MCF-7 cells treated simultaneously with estrogen and ICI 164,384 exhibit markedly lower resistance to Adriamycin compared with cells treated with estrogen alone. In the absence of estrogen, MCF-7 cells transfected with Bcl-2 expression plasmids display a marked increase in resistance to Adriamycin. In the presence of estrogen, MCF-7 cells expressing Bcl-2 antisense transcripts are rendered twice as sensitive to acute Adriamycin cytotoxicity as a control clone. We conclude that estrogen can promote resistance of estrogen receptor bearing human breast cancer cells to chemotherapeutic drugs through a mechanism that involves regulation of the Bcl-2 proto-oncogene.

1 This work was supported by a grant from the Cancer Research Society, Inc., Canada.

2 To whom requests for reprints should be addressed, at Department of Pharmacology, University of Ottawa, 451 Smyth Road, Ottawa, Ontario, Canada K1H 8M5.

Received 2/17/95. Accepted 6/27/95.




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PNAS, March 14, 2000; 97(6): 2703 - 2708.
[Abstract] [Full Text] [PDF]


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