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©The Author(s) 2024.
World J Gastroenterol. Dec 21, 2024; 30(47): 5055-5069
Published online Dec 21, 2024. doi: 10.3748/wjg.v30.i47.5055
Published online Dec 21, 2024. doi: 10.3748/wjg.v30.i47.5055
Figure 4 Enrichment analysis of T cell differentially expressed genes in metabolic dysfunction-associated fatty liver disease hepa tocarcinogenesis.
A: Differentially expressed genes (DEGs) in IL-CD4+ T cells. Left, metabolic dysfunction-associated fatty liver (MAFL) vs normal control (NC); Right, hepatocellular carcinoma (HCC) vs metabolic dysfunction-associated steatohepatitis (MASH); B: DEGs in IL-CD8+ T cells. Left, MAFL vs NC; Right, HCC vs MASH; C: Top 10 DEGs in IL-CD4+ T cells. Left, MAFL vs NC; Right, HCC vs MASHc; D: Top 10 DEGs in IL-CD8+ T cells. Left, MAFL vs NC; Right, HCC vs MASH; E: Gene Ontology (GO) analysis of DEGs; F: KEGG pathway with distribution of the corresponding GO terms of the top 332 features in hepatocarcinogenesis. aP < 0.05, compared with the NC group; NC: Normal control.
- Citation: Wang LL, Lu YM, Wang YH, Wang YF, Fang RF, Sai WL, Yao DF, Yao M. Carnitine palmitoyltransferase-II inactivity promotes malignant progression of metabolic dysfunction-associated fatty liver disease via liver cancer stem cell activation. World J Gastroenterol 2024; 30(47): 5055-5069
- URL: https://www.wjgnet.com/1007-9327/full/v30/i47/5055.htm
- DOI: https://dx.doi.org/10.3748/wjg.v30.i47.5055