Fig. 5

EGFR-T790M secondary mutation upregulates PD-L1 expression in tumour cells through the PI3K/Akt, MAPK, and NF-kappa B signal pathways. a-d 293FT cells were transfected with control vector plasmid (NC), EGFR-19Del (19Del), or EGFR-T790M (T790M) mutation plasmids for 48–72 h, then treated with/without gefitinib for a further 24 h. All the cells were harvested and analyzed by western blotting, RT-qPCR and flow cytometry. Bars indicate SD. * P < 0.05; ** P < 0.01. e 293FT cells were transfected as described above for 48 h, and then treated with TAK-733 (TAK, 0.3 μmol/L) or PF-04691502 (PF, 0.3 μmol/L) for an additional 12 h. PD-L1 expression was evaluated by flow cytometry. Bars indicate SD. * P < 0.05; ** P < 0.01. f H1975 cells were treated with TAK-733(0.3 μmol/L), PF-04691502(0.3 μmol/L), or IMD 0354 (IMD, 1 μmol/L) for 24 h and PD-L1 expression was evaluated by flow cytometry. Bars indicate SD. * P < 0.05; ** P < 0.01. All experiments were performed at least thrice