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Fig. 2 | Molecular Cancer

Fig. 2

From: EGFR-TKI resistance promotes immune escape in lung cancer via increased PD-L1 expression

Fig. 2

HGF upregulates PD-L1 expression by activating PI3K/Akt and MAPK signaling pathway, but not NF-kappa B signaling pathway to promote the phosphorylation and activation of AP-1 in EGFR mutant NSCLC cells. a The correlation coefficient between PD-L1 (CD274) and HGF in lung adenocarcinoma based on the TCGA datasets (Lung Adenocarcinoma, PanCancer Atlas, and Provisional). * P < 0.05; ** P < 0.01. b PC-9 and HCC827 cells were treated with HGF (50 ng/L) for different periods of time, then harvested and measured by flow cytometry to evaluate the expression of PD-L1. c and d PC-9 and HCC827 cells were pre-treated with TAK-733 (TAK, 0.3 μmol/L) or PF-04691502 (PF, 0.3 μmol/L) for 6 h, then stimulated with HGF (50 ng/L) or PBS for an additional 6 h. Cells were harvested and analyzed by western blotting and flow cytometry. Bars indicate SD,* P < 0.05; ** P < 0.01. e HGF moderates the activation and cytotoxic effect of T lymphocytes, and anti-PD-L1 antibodies restores their cytotoxicity. HCC827 cells were pretreated with or without HGF (50 ng/L), anti-PD-L1 antibodies (10 μg/mL) or control IgG for an hour. Then all the cells were co-cultured with human PBMC for 72 h at an effector/target cell ratio = 6:1. The percentage of CD3+/CD4+, CD3+/CD8+ cells in the co-culture system was analysed by flow cytometry. f PC-9 and HCC827 cells were transfected with c-Jun Si-RNA for 72 h, then stimulated with HGF (50 ng/L) or PBS for an additional 6 h. Cells were harvested and analysed by Western blotting. All experiments were performed at least three times

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