Fig. 6: Inhibition of EZH2 activity reverses ERα expression and sensitizes tumors to endocrine therapy.

A, B Western blotting showing the expression of the indicated protein after different treatment in HP5008 cells (A) and 545 cells (B). C, D Effect of EZH2 inhibition on tamoxifen sensitivity in HP5008 (C) and 545 (D) cells with or without dox-induced Rad51b knockout. IC₅₀ values for tamoxifen are indicated. Data are presented as means ± SEM of three independent experiments. E The strategy for establishing tumor slice culture system to investigate the effects of EZH2 inhibitor together with tamoxifen in Rad51b-knockout TNBC tumor. F Visual antitumor response in tumor slice culture system after 1 week treatment revealed by MTT analysis and representative quantified results (G). Data are presented as the means ± SEM, with statistical significance among groups determined by a one-way ANOVA test. H The strategy for establishing mouse models for in vivo ERα signaling detection. I Representative images and quantitation analysis (J) of bioluminescence signals from Day 1–9 of tumor-bearing mice treated with or without dox to induce Rad51b knockout and EZH2 inhibitors treatment. K Summary of ERα, PR and Her2 abundance in tumors from each group measured by IHC analysis. L The strategy for establishing mouse models for in vivo investigation of the effects of combination therapy. Tumor images (M), tumor weight (N), spleen weight (O), and body weight change (P) of mice in each group. Data are presented as the means ± SEM with statistical significance among groups determined by a one-way ANOVA test.