Cicek Gercel-Taylor1, Anna K Feitelson, Douglas D Taylor. 1. Department of Obstetrics, Gynecology and Women's Health, University of Louisville, School of Medicine, Louisville, KY 40202, USA. cgtayl01@gwise.louisville.edu
Abstract
BACKGROUND: Survival from ovarian cancer has not changed significantly in the past twenty years requiring development of additional treatment protocols. We studied the effect of genistein and daidzein on ovarian cancer cell growth. MATERIALS AND METHODS: Five ovarian cancer cell lines from Stage IIIC disease were evaluated. Sulforhodamine B and colony formation assays were used to analyze growth inhibitory effects of genistein and daidzein alone and with cisplatin, paclitaxel or topotecan. Apoptosis induction was studied by determining caspase-3 activity. RESULTS: Inhibition of growth (50-80%), colony formation and colony size was seen at 144 microm of genistein, 0-23% reduction was demonstrated at 9 microm. At 144 microm, the colony size was inhibited >75%; at 9 microm 4/5 cell lines had >50% reduction. Caspase-3 activity was induced (0.10 to 0.56 pmol/min/microg protein) with all concentrations of genistein. Cisplatin (2-50 microg/ml) and topotecan (0.5-50.0 microm) combined with genistein resulted in a mostly additive effect, paclitaxel (8-200 nM) was slightly less than additive. CONCLUSION: We demonstrate an inhibitory effect of genistein on ovarian cancer cell growth.
BACKGROUND: Survival from ovarian cancer has not changed significantly in the past twenty years requiring development of additional treatment protocols. We studied the effect of genistein and daidzein on ovarian cancer cell growth. MATERIALS AND METHODS: Five ovarian cancer cell lines from Stage IIIC disease were evaluated. Sulforhodamine B and colony formation assays were used to analyze growth inhibitory effects of genistein and daidzein alone and with cisplatin, paclitaxel or topotecan. Apoptosis induction was studied by determining caspase-3 activity. RESULTS: Inhibition of growth (50-80%), colony formation and colony size was seen at 144 microm of genistein, 0-23% reduction was demonstrated at 9 microm. At 144 microm, the colony size was inhibited >75%; at 9 microm 4/5 cell lines had >50% reduction. Caspase-3 activity was induced (0.10 to 0.56 pmol/min/microg protein) with all concentrations of genistein. Cisplatin (2-50 microg/ml) and topotecan (0.5-50.0 microm) combined with genistein resulted in a mostly additive effect, paclitaxel (8-200 nM) was slightly less than additive. CONCLUSION: We demonstrate an inhibitory effect of genistein on ovarian cancer cell growth.
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