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Fig. 6 | BMC Cancer

Fig. 6

From: EIF2A-dependent translational arrest protects leukemia cells from the energetic stress induced by NAMPT inhibition

Fig. 6

Protective role of EIF2A and FK866 induced UPR. a Expression level of LKB1 mRNA, evaluated in Jurkat cells after 120 h of lentiviral transduction with shRNAs expressing the control sequence (scramble) or two LKB1-silencing shRNAs (shLKB1-a and –b), in the upper panel. Cells were transduced for 72 h and then treated with FK866 for 48 h. Viability was measured by MTT assay in comparison with Mock (DMSO) condition, in the lower panel. Mean and SD of a biological triplicate (*, p-value < 0.05). b WB analysis indicated the levels of AMPK, p-AMPK, p-EIF2A, p-4EBP1 in A594 cells expressing LKB1 (LKB1 WT) or transduced with an empty vector (pBABE) treated or not (Mock) with 100 nM FK866 for 48 h, left panel. A549 cells were treated with indicated concentration of FK866 for 48 h and cell viability as shown in dose–response curve was evaluated by MTT assay, right panel. Mean and SD of three biological replicates. c A549 viability after 48 h of treatment with FK866 100 nM in un-transfected (NTC) cells and transfected with EIF2A wild type, EIF2A-S51A, EIF2A-S51D (mean and SD of three experiments,*, p-value < 0.05). d Expression level of BiP mRNA, evaluated in Jurkat cells after 48 h of treatment with FK866 5nM (*, p-value < 0.0005). Mean and SD of a biological triplicate. e WB analysis of MCL1 in Jurkat cells treated with FK866 for 48 h and with the proteasome inhibitor MG132 1 μM for 24 h. MG132 was added after 24 h of FK866 treatment. One representative experiment out of three biological replicates

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