GATA1 Promotes Gemcitabine Resistance in Pancreatic Cancer through Antiapoptotic Pathway
Figure 5
GATA1 inhibits gemcitabine-induced apoptosis through Bcl-XL in vitro. (a) Cell viability curves of CFPAC-1 and PANC-1 cells stably infected with the indicated lentiviruses. Western blot assay of GATA1 and Bcl-XL expression in indicated cells. β-actin was used as a loading control. Cells were treated with a range of concentration of gemcitabine for 48 h before CCK8 assay. (b) Representative images of colony formation assays in stable CFPAC-1 cells lines from (a). The cells were treated with control or gemcitabine (1 μM) for 48 h before seeded into 6-well plates. Relative colony numbers were quantified and compared by t test. (c) Representative images of flow cytometry analysis of apoptosis in CFPAC-1 cells transfected with indicated lentivirus. The cells were treated with or without gemcitabine (5 μm) for 48 h. Statistical analysis of apoptosis rates was shown in the right panel. (d) Western blot analysis of GATA1, Bcl-XL, Bax, cleaved PARP, cleaved caspase 9, and cleaved caspase 3 in CFPAC-1 and PANC-1 infected with the indicated lentivirus. The cells were treated with or without gemcitabine (10 μM for CFPAC-1 and 50 μM for PANC-1) for 48 h before analysis. All data shown are means ± SD of three independent experiments with triplicate each, ; .