Fig. 1

Treatment with either Dex or a selective GR modulator (SGRM) suppresses ER-mediated cell proliferation. a MCF-7 and T-47D cells were treated for 8 days with either vehicle (Veh, ETOH), dexamethasone (Dex, 100 nM), estradiol (E2, 10 nM), or Dex/E2 and total live cells counted. E2 treatment-alone (ER activation) significantly increased cell proliferation compared to either Veh or Dex-alone. Dex/E2 significantly reduced E2-mediated proliferation. There was no difference between Dex and Veh treatment (****p < 0.0001, vs. Veh, two-way ANOVA, Holm-Sidak post hoc test; NS, not significant, n = 4 per group, ± SD). b MCF-7 and T-47D cells were treated with vehicle (ETOH), 10 nM E2, E2/1 μM C134 or E2/1 μM C335 and total live cells counted. GR-selective liganding with C134 or C335 significantly reduced E2-mediated proliferation (****p < 0.0001, vs. E2-alone, two-way ANOVA, Holm-Sidak post hoc test, n = 4 per group, ±SD). c FACS cell cycle analyses were performed and revealed GR-selective liganding significantly inhibited G2 cell cycle progression compared to E2-alone treated cells (**p < 0.01, ***p < 0.001 one-way ANOVA, Tukey’s post hoc test, n = 3 per group, ±SD)