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Programmed Cell Death during Regression of the MCF-7 Human Breast Cancer following Estrogen Ablation¹

The Johns Hopkins Oncology Center, Baltimore, Maryland 21205 [N. K., N. E. D., J. T. I.], and the Division of Endocrinology and Urology, Hershey Medical Center, Hershey, Pennsylvania 17033 [H. F. E.]

To study the mechanism of regression of human mammary cancer following estrogen ablation, estrogen-responsive MCF-7 human mammary adenocarcinoma cells were inoculated into ovariectomized female nude mice supplemented with exogenous 17ß-estradiol (E₂) via an E₂ implant. Implants were then removed when MCF-7 tumors were 400 mm³ in size. Removal of the E₂ implants resulted in a 50% tumor regression by 2 weeks following E₂ ablation. Associated with this regression is a rapid (i.e., within 1 day following E₂ ablation) enhanced expression of the transforming growth factor ß₁ and TRPM-2 genes, two genes the expression of which has been previously demonstrated to be enhanced in a variety of cell types induced to undergo programmed cell death (i.e., apoptosis). The enhanced expression of transforming growth factor ß₁ and TRPM-2 is not a nonspecific response since the expression of other genes, like c-fos, c-H-ras, and pS2, decrease following E₂ ablation. Fragmentation of tumor DNA into nucleosomal oligomers and histological appearance of apoptotic bodies are characteristic early events that precede the dramatic reduction in tumor volume following E₂ ablation. These results demonstrate that the regression of MCF-7 human mammary cancers in nude mice following estrogen ablation is due to a sequence of biochemical and morphological changes that result in both the cessation of cell proliferation and activation of programmed death or apoptosis of these MCF-7 cancer cells. Clarification of the biochemical pathway involved in the activation of this programmed cell death should identify new targets of therapy for even estrogen-independent human mammary cancer cells.

¹ These studies were supported by Department of Health and Human Services Grants CA 50601 and CA 40011. N. E. D. is a recipient of an American Cancer Society Clinical Oncology Career Development Award 90–128 and a Merck Clinician Scientist Award.

² To whom requests for reprints should be addressed, at The Oncology Center, Breast Cancer Laboratories, 422 N. Bond Street, Baltimore, MD 21231.

Received 7/20/90. Accepted 10/10/90.

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