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• W1567174689 abstract "Abstract : The purpose of our investigation was to elucidate the molecular mechanism(s) by which genistein elicits its biological effects on non-tumorigenic and tumorigenic breast epithelial cells. We have recently obtained experimental evidence supporting the differential effect of genistein in our system. We found that genistein causes a greater degree of G2/M arrest and induces apoptosis in malignant cell lines compared to normal breast epithelial cells. After genistein treatment, flow cytometric analysis WAFI revealed a hyperdiploid population in malignant cells that was not observed in normal cells. Cell cycle regulator p2l which is known to be up-regulated by genistein treatment, was greatly induced at RNA and protein levels in normal cells, while its level was only slightly induced in malignant MDA-231 cells and not detectable in malignant MCFl0CAla cells. We also found that there was a greater degree of cell cycle arrest and apoptosis in p21 WAFI %%% cells compared to p21 WAFI +%+ HCTl 16 cells after genistein treatment. Flow cytometric analysis after genistein treatment, showed a significant number of p21 WAFI cells in the hyperdiploid population, which are probably programmed to die through apoptotic processes. Moreover, we found that both malignant and normal p21WAF anti-sense (AS) expressing clones became more sensitive to G2/M arrest after genistein treatment. Flow cytometric analysis showed an increase in the hyperdiploid population in the AS clones. Further evaluation showed an increase in apoptosis in malignant AS clones but not in normal epithelial AS clones. These results suggest that %21 WAFI plays an important role in the differential effects of genistein in breast epithelial cells." @default.
• W1567174689 created "2016-06-24" @default.
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• W1567174689 date "1999-08-01" @default.
• W1567174689 modified "2023-09-25" @default.
• W1567174689 title "Soy Metabolites, Isoflavones in Cell Growth and Apoptosis" @default.
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• W1567174689 doi "https://doi.org/10.21236/ada374128" @default.
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