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. 2023 Mar 4;14(3):178. doi: 10.1038/s41419-023-05702-6

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© The Author(s) 2023

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Correlation between SP1 and TRIM56 expression levels in The Cancer Genome Atlas (TCGA) (A) and CGGA_mRNAseq_693 (B) cohorts. Relative TRIM56 mRNA expression levels following GATA1, IRF2, SP1, and YY1 overexpression in U251 (C) and U87 (D) cells. E SP1 overexpression in U87 and U251 cells upregulated TRIM56 expression. F The sequence motif of TRIM56 promoter for SP1 binding, analyzed via JASPAR. G Four truncations of the TRIM56 promoter were integrated into pGL3 plasmids. H Relative promoter activity of truncations in U251 cells. I Schematic depiction of wild type and mutant SP1 binding sites in the TRIM56 promoter. J Relative activity of the mutant TRIM56 promoter in SP1-overexpressing U251 cells. K Relative activity of the mutant TRIM56 promoter in SP1-knockdown U87 cells. L ChIP-qPCR analysis of SP1 bound on the promoter of TRIM56 in U251 cells. M Representative immunohistochemical staining displaying the relationship between TRIM56 expression and SP1, IQGAP1 expression in glioma samples, respectively.