Fig. 7

PM2.5 activates the expression of transcription factor Sp1 which enhances the transcription of DLAT. A PM2.5 promoted Sp1 expression in a dose-response manner in BEAS-2B cells. B PM2.5 enhanced the expression of Sp1 in lung tissues of rats. C PM2.5 increased the expression of Sp1 protein in lung tissues of rats. D, E The expression level of Sp1 was positively correlated with that of DLAT in LUAD (lung adenocarcinoma) and LUSC (lung squamous carcinoma) in TCGA dataset. F In silico analysis identified Sp1 putative binding sites in the promoter region of DLAT. G ChIP assay showed the binding of Sp1 with DLAT promoter region. H Potential binding sequences for Sp1 were found in the DLAT promoter region. I Luciferase reporter assay verified that the binding of Sp1 with wild-type DLAT promoter significantly increased the luciferase activity. While binding of Sp1 with mutant DLAT promoter did not changes the intensity of luciferase signals. J Schematic view for the mechanisms of action of DLAT-mediated glycolysis reprograming in PM2.5-induced carcinogenesis. *P<0.05, **P<0.01, ***P<0.001.