Scientific Program (Oral Abstracts) | Poster Abstracts | Speaker List
SECOND INTERNATIONAL SYMPOSIUM
ON THE ROLE OF SOY
IN PREVENTING AND TREATING CHRONIC DISEASESeptember 15-18, 1996
Brussells, Belgium
SCIENTIFIC PROGRAM
(Oral Abstracts)Soy and Cancer
Soybean Anticarcinogens / Anticancer MechanismsGenistein Can Induce MCF-7 Breast Carcinoma Cell Differentiation or Death, Depending on the Dose.
Constantinou A., Krygier A., Murley J., Runyan C., Mehta R.R., Kamath N., and Grdina, D. Department of Surgical Oncology, University of Illinois at Chicago, Chicago, IL 60612 [C.A., K.A., R.C., M.R.R., K.N.], and Center for Mechanistic Biology and Biotechnology, Argonne National Laboratory, Argonne, IL, 60439 [G.D., M.J.].Recent studies in animal models of mammary carcinogenesis identified the phytoestrogen genistein as a chemopreventive agent. The objectives of the present studies are: a) to explore the value of genistein in the prevention of human breast carcinogenesis, b) to explore its value in the treatment of human breast cancer, and c) to identify its molecular mechanism of action. Human breast carcinoma MCF-7 cells treated for nine days with 30 M of genistein became terminally differentiated, as judged by the induction of intra-cytroplasmic casein and lipids. No measurable changes in phosphotyrosine-containing peptides or in cell cycle progression were evident under these treatment conditions. Genistein at 150 M caused cell death accompanied by cell cycle delay in the G2-M phase. Twenty-four hours post-treatments, 47% of the cells were accumulated at G2-M, compared to 20% in the untreated controls. At these cytotoxic concentrations, genistein caused little or no change in the steady-state levels of wild-type tumor suppressor p53 protein, indicating that MCF-7 cell death was not mediated through the apoptotic pathway. Mutant P53, expressed in MDA-MB-468 breast carcinoma cells, was down-regulated 24 hours post-genistein treatment. These data suggest that genistein, at low concentrations, may interfere with carcinogenesis by promoting mammary cell maturation. The introduction of high intracellular concentrations, however, caused cell death, suggesting that genistein may find applications in cancer treatment. (Supported by NIH grants CA 56785 and CA 62184).
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