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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. 3 — In the TCGA (A, B) and CGGA_mRNAseq_325 (C, D) cohorts, glioma samples were divided into TRIM56 high- and low-expression groups based on median TRIM56 expression. GSEA results revealed that the KEGG_FOCAL_ADHESION and KEGG_REGULATION_OF_ACTIN_CYTOSKELETON pathways were enriched in the TRIM56 high-expression group (CGGA: CGGA_mRNAseq_325 database). E–H Upon grouping the samples as described above, GSEA results revealed that glioma invasion and cancer cell invasion gene sets were enriched in the TRIM56 high-expression group. I Functional enrichment analysis of differentially expressed genes between TRIM56 knockdown cells and control cells in the Metascape platform.