Fig. 7

miR-155 and miR-146a collectively modulate EGFR–NF-κB signaling. a Predicted miR-155 binding site in 3’ UTR of EGFR. Eight mutated nucleotides of the target site were indicated in red. b HEK-293T cells were co-transfected with miR-155 mimics or miR-ctrl, along with the wild-type or mutated EGFR 3’ UTR luciferase reporter plasmid (EGFR 3’ UTR-MUT1). c Predicted miR-146a binding site in 3’ UTR of EGFR. Six mutated nucleotides of the target site are indicated in red. d HEK-293T cells were co-transfected with miR-146a mimics or miR-ctrl, along with the wild-type or mutated EGFR 3’ UTR luciferase reporter plasmid (EGFR 3’ UTR-MUT2). e and f The mRNA and protein levels of EGFR were determined in U251 cells after 24 h of transfection with miR-155, miR-146a, anti-miR-155, anti-miR-155, or their corresponding control oligonucleotides. g and h The mRNA and protein levels of EGFR were determined in PCN033-infected U251 cells. i and j U251 cells were infected with PCN033 or mock-infected in the presence of increasing concentrations of the EGFR inhibitor AG1478, and the protein levels of NF-κB p65 and phosphorylated p65 were determined by Western blotting, while the mRNA levels of IL-1β, IL-6, TNF-α, MCP-1, and MIP-2 were determined by qPCR. All data were represented as mean + SD (n = 3/group). Statistical analysis was carried out by Student’s t test or one-way ANOVA. p < 0.05 was considered statistically significant; p < 0.01 and p < 0.001 indicated extremely significant differences