Fig. 8

a MFX and CFX causes ERK mediated apoptosis in pancreatic cancer cells. (i) Abolishment of apoptosis in MIA PaCa-2 cells as assessed by annexin-V assay. Left panel represents the bar graph where vertical axis represents % apoptotic cells and horizontal axis represents MFX and CFX concentration in μg/ml, and U0126 concentration in μM. Bar graph represents mean ± SEM from three independent experiments. *p < 0.01 versus MFX/CFX alone. Right panel shows western blot for the knockdown efficiency of ERK1/2 inhibitor (U0126). (ii) Abolishment of apoptosis in Panc-1 cells as assessed by annexin-V assay. Left panel represents the bar graph where vertical axis represents % apoptotic cells and horizontal axis represents MFX and CFX concentration in μg/ml, and U0126 concentration in μM. Bar graph represents mean ± SEM from three independent experiments. *p < 0.01 versus MFX/CFX alone. Right panel shows western blot for the knockdown efficiency of ERK1/2 inhibitor (U0126). (1) represents untreated control cells, (2) U0126 treated cells, (3) cells treated with 400 μg/ml of MFX alone, (4) U0126 treated cells with 400 μg/ml of MFX, (5) cells treated with 400 μg/ml of CFX alone, (6) U0126 treated cells with 400 μg/ml of CFX. b MFX and CFX augment apoptotic effects of cisplatin via ERK activation in pancreatic cancer cells. (i) Annexin-V assay of MIA PaCa-2 cells treated either alone with MFX and CFX (400 μg/ml) or in combination with cisplatin(CDDP) 20 μM for 48 h. (ii) Western blot analysis for pERK expression in MIA PaCa-2 cells treated either with MFX, CFX & CDDP alone or in combination for 48 h. Bar Graph represents the mean ± SEM of the fold change from three independent experiments. *p < 0.01, #p < 0.05 versus control