Role of Asxl2 in non‑alcoholic steatohepatitis‑related hepatocellular carcinoma developed from diabetes.

摘要: The present study investigated the mechanism(s) of non‑alcoholic steatohepatitis‑related hepatocellular carcinoma (NASH‑HCC) developed from diabetes. Streptozotocin and a high‑fat diet (STZ‑HFD) were used to induce NASH‑HCC in ApoE‑/‑ mice. Mouse liver functions evaluated by H&E staining, liver/body weight serum biochemical analysis. expression levels inflammation‑associated factors determined RT‑qPCR. Gene profiles related molecular pathways examined principal component analysis, heatmap, gene ontology KEGG pathway enrichment Differentially expressed genes (DEGs) tumor tissues confirmed Asxl2 human NASH‑HCC, other HCC cells was measured western blot (WB analysis) For SNU‑182 transfected with siAsxl2 or Hep3B overexpression, cell proliferation, cycle, migration invasion respectively CCK‑8 assays, flow cytometry, wounding healing Transwell assays. metastasis‑ cycle‑related proteins WB analysis model mice exhibited protrusion severe steatosis. blood glucose concentration, alanine aminotransferase (ALT), aspartate (AST) low‑density lipoprotein (LDL), total bile acid (TBA) interleukin (IL)‑6, necrosis factor (TNF)‑α, glypican 3 (GPC3) transforming growth (TGF)‑β all increased DEGs mainly chromosome organization, cycle mitogen‑activated kinase (MAPK) pathway. significantly downregulated cells, this regulated growth, invasion. pattern, signaling differed those normal tissues. Additionally, downregulation may play potential role development patients