Fig. 2

SETDB1 modulates tamoxifen response via Akt activation. A Gene set enrichment analysis of Akt signaling and tamoxifen resistance gene signatures upon SETDB1 KD were analyzed using RNA-seq data. B, C Effect of SETDB1 KD on selective tamoxifen resistance genes shown by heatmap (B) were validated using RT-qPCR analysis (C). D Effect of tamoxifen on the cell viability of control-sh and SETDB1-sh ZR75 and MCF7 cells was determined using the MTT assay. E Effect of tamoxifen on colony formation of control-sh and SETDB1-sh cells. Model cells were cultured in 5% DCC medium for 48 h, then treated with E2 (10⁻⁸ M) or Tamoxifen (2.5 μM). Shown are the results from one representative experiment of three replicates. F ZR75 and MCF7 cells stably expressing control-sh or SETDB1-sh were serum starved for 24 h and stimulated with 10% serum for 15 min. Effect of SETDB1-KD on Akt phosphorylation was analyzed by Western blotting. G ZR75 and MCF7 cells stably expressing control vector or SETDB1 vector were serum starved for 24 h and stimulated with 10% serum for 0, 15, and 30 min. Effect of SETDB1 overexpression on Akt downstream signaling was determined by Western blotting. Data was represented as mean ± SEM. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001