Fig. 3

The effects of selective and nonselective ER ligands and soy-derived isoflavonoids on cisplatin cytotoxicity in D283 Med cells. a Representative images of surviving coomassie blue stained colonies from D283 Med cultures cotreated with 4 μM cisplatin and either vehicle, 10 nM E2, 10 nM PPT or 10 nM DPN. b Quantification of colony number from clonogenic assays of D283 Med cells cotreated with 4 μM cisplatin and vehicle, or 10 nM of E2 (n = 18), PPT (n = 7), DPN (n = 8), or 10 nM of genistein, daidzein, or s-equol (n = 6 for each isoflavonoid group). c Concentration response analysis of estrogenic inhibition of caspase 3 activity by increasing concentrations of s-equol, daidzein, or genistein in D283 Med cultures. Control cultures exposed to 0.01% DMSO vehicle or 10 nM E2 were treated and analyzed in parallel. Caspase activity was quantified following a 48 h incubation period. Results were normalized to the relative caspase 3 activity of the vehicle control and expressed as mean percent of the effects for 10 nM E2. The number of samples in each group was n = 10-12. d Representative images of surviving coomassie blue stained colonies from D283 Med cultures cotreated with 4 μM cisplatin and either vehicle, 10 nM E2, 10 nM fulvestrant (ICI), or 10 nM E2 and 10 nM fulvestrant (ICI/E2). e Quantification of colony number from clonogenic assays of D283 Med cells cotreated with 4 μM cisplatin and either vehicle (n = 12), 10 nM E2 (n = 12), 10 nM fulvestrant (ICI; n = 8), 10 nM E2 and 10 nM fulvestrant (ICI/E2; n = 7), 1 μM 4-OH tamoxifen with and without 10 nM E2 (n = 8), or 5 μM PHTPP with and without E2 (n = 8). All results are expressed as mean ± SEM. Significant differences from the control group was determined by one-way ANOVA followed by Holm-Sidak’s multiple comparisons tests which is indicated above the error bars: * p ≤ .05