Supplementary Figure 7: Combination treatment increases caspase 3/7 activity in glioma cells.
From: A TNF–JNK–Axl–ERK signaling axis mediates primary resistance to EGFR inhibition in glioblastoma
(a) GBM9 cells were treated by erlotinib and/or SP600125, U1026 for 72 hours followed by Caspase-Glo 3/7 Assay. Caspase3/7 activity was evaluated in GBM9 cells exposed to erlotinib plus SP600125. Similar results were obtained using a combination of erlotinib and U1026. Erlotinib vs erlotinib+SP600125: P =0.001, t=8.66, d.f.=4; Erlotinib vs erlotinib+U0126: P =0.0002, t=13.24, d.f.=4. Similar procedures were performed in b-f and similar results were obtained. (b) Erlotinib vs erlotinib+R428: P =0.0004, t=10.76, d.f.=4; Erlotinib vs erlotinib+thalidomide: P=0.0004, t=10.64, d.f.=4. (c) Erlotinib vs erlotinib+SP600125: P<0.0001, t=21.41, d.f.=4; Erlotinib vs erlotinib+U1026: P =0.0007, t=9.49, d.f.=4. (d) Erlotinib vs erlotinib+R428: P=0.0001, t=14.8, d.f.=4; Erlotinib vs erlotinib+T: P <0.0001, t=16.77, d.f.=4. (e) Erlotinib vs erlotinib+enbrel: P =0.0096, t=8.72, d.f.=4. (f) Erlotinib vs erlotinib+enbrel: P =0.0017, t=7.43, d.f.=4. Data are presented as mean±s.e.m; **P<0.01, ***P<0.001, ****P<0.0001 from two-tailed unpaired Student's t-test (n =3 biologically independent experimental replicates).
