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Fig. 5 | Molecular Cancer

Fig. 5

From: Activation of the PI3K/AKT signaling pathway by ARNTL2 enhances cellular glycolysis and sensitizes pancreatic adenocarcinoma to erlotinib

Fig. 5

ARNTL2 knockdown limits the response of PC cells to erlotinib. A-D Cell proliferation of PANC-1 cells incubated with shRNA-1, shRNA-2, and shRNA-4 against ARNTL2 or control (NC) and treated for 72 h with erlotinib at 2.5 μM, 5 μM, and 10 μM, respectively; E–F ARNTL2 knockdown efficiency of the shRNAs was measured by western blotting and q-PCR, respectively; G-H Colony-formation assay of PANC-1 cells incubated with shRNA-1, shRNA-2 and shRNA-4 against ARNTL2 or control (NC) were grown in the absence or presence of erlotinib at the indicated concentrations for 7–10 days, fixed and stained; I Synergistic response to erlotinib treatment in PANC-1 cells incubated with shRNA-1, shRNA-2 and shRNA-4 against ARNTL2 or control (NC); J IC50 assay of erlotinib in PANC-1 cells incubated with shRNA-1, shRNA-2 and shRNA-4 against ARNTL2 or control (NC). K-L Flow cytometry analysis of erlotinib-induced cell apoptosis in ARNTL2 knockdown PANC-1 cells treated with erlotinib and stained with Annexin V-APC-633/PI. All data are presented as the mean ± SEM of triplicate experiments. *p < 0.05; **p < 0.01; ***p < 0.001 by repeated measures with Student’s t test

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