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. 2022 Apr 27;8(17):eabh3635. doi: 10.1126/sciadv.abh3635

Fig. 6. MYCi975 enhances the efficacy of antihormone therapy.

Fig. 6.

(A) Immunoblot showing loss of FOXM1, FOXA1, AR, and AR variant protein levels in sonicated nuclear fractions of MYCi975-treated 22Rv1 cells. Replicates (1 and 2) represent biological replicates of cells treated with 10 μM MYCi975 for 48 hours. (B) Genome browser tracks of MYC (green) ChIP-seq data at the FOXA1, FOXM1, and AR gene loci in MYCi975-treated 22Rv1 cells. TSS of each gene is indicated by an arrow. (C) Representative 4 × 5 dose-response matrices showing percentage viability (left) and Bliss index (right) analysis of predicted versus observed cell viability of prostate cancer cells (LNCaP, C4-2B, and 22RV1) treated with MYCi975 and ENZ or the breast cancer line MCF-7 treated with MYCi975 and 4-OHT (n = 3). Bliss scores > 0 indicate synergy, scores close to zero indicate additivity, and scores < 0 denote antagonism. (D) Fold change tumor volumes of 22Rv1 xenografts in nude mice treated with MYCi975 (100 mg/kg BID p.o.) or vehicle, 5 days a week for 3 weeks. n = 4 to 7 grafts per group (from three to four mice). (E) Fold change tumor volumes of 22Rv1 xenografts in nude mice treated with MYCi975 (100 mg/kg QD p.o.), ENZ (25 mg/kg QD i.p.), combination of MYCi975/ENZ, or vehicle for 18 days. n = 7 to 8 grafts per group (from four to five mice). Error bars represent means ± SEM and analyzed by two-way analysis of variance (ANOVA) in GraphPad Prism for (D) and (E) (*P < 0.05; ****P < 0.0001).