Research Paper Volume 16, Issue 9 pp 7704—7732
Immune cell senescence and exhaustion promote the occurrence of liver metastasis in colorectal cancer by regulating epithelial-mesenchymal transition
Figure 4. Enrichment analysis results. (A, B) Functional Gene Set Enrichment Analysis (fGSEA) for senescent-like myeloid cells (SMCs) subtypes from primary and liver metastasis colorectal cancer tissues, resulting in differential Hallmark signaling pathways (A) with selective GSEA plots (B). (C, D) fGSEA analysis for exhausted T cells (TEXs) subtypes from primary and liver metastasis colorectal cancer tissues, leading to differential Hallmark signaling pathways (C) with specific GSEA plots (D). (E–H) Enrichment analysis results for SMCs subtypes from primary and liver metastasis colorectal cancer tissues, based on Gene Ontology (GO) biological functions (E) and Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathways (F), further analyzed for metabolic pathway enrichment through KEGG (G) and Reactome (H) pathways. (I–L) Enrichment analysis results for TEXs subtypes from primary and liver metastasis colorectal cancer tissues, based on GO biological functions (I) and KEGG signaling pathways (J), further analyzed for metabolic pathway enrichment through KEGG (K) and Reactome (L) pathways.