Skip to main content
Fig. 6 | Journal of Translational Medicine

Fig. 6

From: IL-1RA promotes oral squamous cell carcinoma malignancy through mitochondrial metabolism-mediated EGFR/JNK/SOX2 pathway

Fig. 6

Involvement of mitochondrial metabolism in IL-1RA-associated EGFR/JNK activation and SOX2 expression. AB Up-regulated phosphorylation of EGFR and JNK was shown by phospho-kinase proteome array screening for the phosphorylation status of a set of kinases, with duplicate detection for each kinase, in OECM-1 cells with overexpression of IL-1RA in (A), which was further confirmed by Western blot in (B). C Protein expression of phosphorylated EGFR and JNK, along with their unphosphorylated forms, in OECM-1 cells with overexpression of IL-1RA and control cells was examined by Western blot in the presence or absence of metformin. D Protein expression of phosphorylated EGFR and JNK, along with their unphosphorylated forms, and SOX2 in OECM-1 cells with overexpression of IL-1RA and control cells was examined by Western blot in the presence or absence of gefitinib. Data were presented as mean ± SD from three independent experiments in (BD). *, p < 0.05; **, p < 0.01; ***, p < 0.001. EF Correlation between IL-1RA expression and phosphorylation of EGFR (E) and JNK (F) in OSCC tumor tissues from patients was analyzed according to IHC scoring, and was evaluated by Pearson correlation (r). Met., metformin; Gef., gefitinib; p-EGFR, phosphorylated EGFR; p-JNK, phosphorylated JNK; EV, empty vector; IL-1RA-OE, overexpression of IL-1RA

Back to article page