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BML-275, an AMPK inhibitor, induces DNA damage, G2/M arrest and apoptosis in human pancreatic cancer cells

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Figure 1. Measurements of AMPK activity in human pancreatic cancer  cell lines (AsPC-1, Panc-1, MIA-PaCa2, Capan-1, CFPAC-1, Colo-357 and  BxPC-3) and immortal human pancreatic duct epithelial cell line (HPDE6-C7)
Figure 2. BML-275 inhibits cell viability in human pancreatic cancer cells. (A) An MTT assay of MIA PaCa-2, CFPAC-1, Panc-1 and AsPC-1 cells treated with  various concentrations of BML-275 (0, 1, 3, 5 and/or 10 µM) for 48 h were used to determine cell viab
Figure 5. BML-275 inhibits AMPK activity. WB of MIA PaCa-2 and Panc-1  cells pretreated with 10 µM A769662 for 6 h and further treated with BML-275  in different concentrations (0, 5, 10 and/or 15 µM) for 24 h were used to  deter-mine the total and phospho
Figure 6. ROS generation is critically required for apoptotic cell death by BML-275. (A) The result of ROS generation analysis of MIA PaCa-2 and Panc-1 cells  treated with 10 µM BML-275 in different time intervals (0, 6, 12 and/or 24 h) and treated with DC
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