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. 2022 Jul 22;41:229. doi: 10.1186/s13046-022-02437-8

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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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.