Supplementary Figure S2 from Integration of Downstream Signals of Insulin-like Growth Factor-1 Receptor by Endoplasmic Reticulum Stress for Estrogen-Induced Growth or Apoptosis in Breast Cancer Cells

(A) The JNK inhibitor effectively blocked phosphorylation of JNK. MCF-7:2A cells were treated with vehicle (0.1% DMSO) or SP600125 (10-5 mol/L) for 24 hours. p-JNK was examined by Western blot. Total JNK was measured as loading control. (B) The JNK inhibitor could not block E2-induced apoptosis in MCF-7:2A cells. MCF-7:2A cells were treated with vehicle (0.1% DMSO; con), E2 (10-9 mol/L), SP600125 (10-5 mol/L), and E2 (10-9 mol/L) plus SP600125 (10-5 mol/L) for 6 days. Annexin V binding assay was used to detect apoptosis. p<0.001, ** compared with control. (C) Cell viability after E2 combination with the JNK inhibitor. MCF-7:2A cells were treated with vehicle (0.1% DMSO), E2 (10-9 mol/L), SP600125 (10-5 mol/L), and E2 (10-9 mol/L) plus SP600125 (10-5 mol/L). Cells were harvested after 7 days treatment and cell viability was quantitated by determination of total DNA. p<0.001, ** compared with control.