MOESM1 of Estrogen receptor coregulator binding modulator (ERX-11) enhances the activity of CDK4/6 inhibitors against estrogen receptor-positive breast cancers

Additional file 1: Figure S1. (A) MCF-7 or (B) T-47D cells were stimulated with E2 (10-8M) for 3 days in the presence or absence of 1 μM of ERX-11 or cisplatin or paclitaxel or gemcitabine or in combination and the cell viability was measured by Cell Titre-Glo Luminescent assay. Figure S2. ZR-75, T-47D, MCF-7/TamR, ZR-75-ESR1-MT-Y537S and ZR-75-ESR1-MT-D538G cells were stimulated with E2 (10-8M) for 7 days in the presence or absence of ERX-11 (0.5μM) or palbociclib (0.5μM) or in combination with indicated concentrations of ERX-11 and the cell viability was measured by MTT assay. Figure S3. Equal number of ZR-75, ZR-75-ESR1-MT-Y537S and ZR-75-ESR1-MT-D538G cells were plated and treated with ERX-11 (500nM) or palbociclib (50 nM) or abemaciclib (50nM) or ribociclib (50nM) or combination and clonogenic (survival) assays were performed after 14 days. Figure S4. (A) Parental MCF-7 or ribociclib resistant MCF-7/RR cells were stimulated with E2 (10-8M) for 5 days in the presence or absence of ERX-11 (1, 5, 10 μM) or ribociclib (1 μM) or in combination and the cell viability was measured by Cell Titer-Glo Luminescent assay. (B) MCF-7 or (C) MCF-7/RR cells were treated with E2 (10-8M) for 5 days in the presence or absence of ERX-11 (1, 2, 5 μM) or ICI (0.2, 0.4, 1 μM). Figure S10. Schematic representation of model for mechanisms of ERX-11+palbociclib therapy.