Extended Data Fig. 2. ESR1 loss is not mediated by epigenetic repressive mechanisms, and corin treatments in parental and endocrine resistant MCF7 cells.
a-b, WB of PRC2 subunits (EZH2 and SUZ12) and ERα from whole cell extracts of FM and reprogrammed (Repro.) cells cultured for 3 and 5 days in the presence of 1µM or 5µM of PRC2 inhibitors EPZ6438 (a) and GSK343 (b). Total H3K27me3, the primary substrate of EZH2, decreased after PRC2 inhibition. c, ERα WB from whole cell extracts of FM and reprogrammed cells cultured for 3 and 6 days in the presence of vehicle (DMSO), 1µM, 5µM, or 10µM of the G9A inhibitor, UNC0638. d, ERα WB from whole cell extracts of FM and reprogrammed cells cultured for 6 days in vehicle (DMSO), 5µM, or 10µM of the DNMT inhibitor, decitabine (Deci.), 0.5µM of the HDAC inhibitor, SAHA, or in combination. e, Proliferation of reprogrammed cells treated with 5µM DMSO (vehicle) or two LSD1 enzymatic inhibitors (MCC2580, DPP38003) for 6 days, n = 3 biological independent replicates, data are presented as mean values + SEM, p-value < 0.05 for treatment with MCC2580 on day 6 (two-way ANOVA). f, Growth curves of 2 × 105 FM, LTED, TamR, and FulR MCF7 cultured with DMSO (vehicle) or 500nM corin for 7 days, n = 3 independent experiments (except FulR cells, n =2 independent experiments), Data are presented as mean values + SEM, p-value < 0.001 (two-way ANOVA). Uncropped images are available as source data.