Figure 4 | Scientific Reports

Figure 4

From: EGFR-L858R mutant enhances lung adenocarcinoma cell invasive ability and promotes malignant pleural effusion formation through activation of the CXCL12-CXCR4 pathway

Figure 4

EGFR-L858R–dependent up-regulation of CXCR4 expression in lung cancer cells is mediated by the ERK signaling pathway.

H1299-EGFR-L858R cells were serum-starved for 24 hours, preincubated for 1 hour with or without pharmacological inhibitors of individual pathways and then stimulated with EGF (40 ng/ml) for 5 minutes. (a) Surface CXCR4 protein expression was evaluated by flow cytometry. CXCR4 expression data are presented as MFI ratio and are expressed as means ± SD of three independent experiments (*P < 0.01). P-values (two-sided) were determined using Student’s t-test. (b) The effective inhibition concentration of EGFR inhibitor AG1478 (10 μM) were used and the phosphorylated and total protein of EGFR, ERK, AKT and STAT3 were detected by Western blotting in H1299-EGFR-L858R cells with or without EGF stimulation. The full size blots were shown in the Supplementary Figure S4 and band of interest is indicated with an arrow. The samples derive from the same experiment and that blots were processed in parallel. (c) The effective inhibition concentration of ERK inhibitor U0126 (10 μM) were used and the phosphorylated and total protein of EGFR, ERK, AKT and STAT3 were detected by Western blotting in H1299-EGFR-L858R cells with or without EGF stimulation. The full size blots were shown in the Supplementary Figure S4 and band of interest is indicated with an arrow. The samples derive from the same experiment and that blots were processed in parallel.

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