Fig. 6

AKT and ERK signaling pathways contributed to synergistic interaction between apigenin and ABT-263. a H1975 and HCC827 cells were treated with Apg (15 µM), ABT (2 µM) alone or in combination for 1 day. Cells were harvested, and the major downstream pathway molecules of EGFR were examined by Western blotting. b H1975 and HCC827 cells were treated with 15 µM Apg for up to 12 h, the total and phosphorylated AKT, ERK1/2, STAT3 and EGFR were analyzed by the immunoblotting. c H1975 and HCC827 cells were treated with MK-2206 (1 µM) and ABT (2 µM), alone or in combination for 1 day. The apoptotic cell death were analyzed (left), the total and phosphorylated-AKT and cleaved caspase 3 were detected by Western blotting (right). d H1975 and HCC827 cells were treated with PD0325901 (2 µM) and ABT (2 µM), alone or in combination for 1 day. The apoptotic death rates were analyzed (left), and the total and phosphorylated-ERK1/2 and cleaved caspase 3 were detected by Western blotting (right). e H1975 cells transfected with ca-AKT1 or empty vector were treated with DMSO or the combination of Apg and ABT for 24 h. The apoptotic death rates were analyzed (left), AKT1 and cleaved caspase 3 were determined by Western blotting (right). f H1975 cells transfected with ca-MEK1 or empty vector were treated with DMSO or the combination of Apg and ABT for 24 h. The apoptotic death rates were analyzed (left), MEK1 and cleaved caspase 3 were detected by Western blotting (right). g H1975 cells cotransfected with ca-MEK1and ca-AKT1 or empty vector were treated with DMSO or the combination of Apg and ABT for 24 h. The apoptotic death rates were analyzed (left), and p-AKT, p-ERK, cleaved caspase 3 and Noxa were detected by Western blotting (right). The data represents mean ± SD (n = 3). *p < 0.05