Lipid metabolic reprogramming in colorectal cancer: Insights to mechanisms and therapeutics

Figure 3 Lipid metabolic alterations in colorectal cancer cells. Hypoxia and signal pathway including transforming growth factor-β1 and phosphatidylinositol 3-kinase/protein kinase B attributes to the reprogramming lipid metabolism in colorectal cancer cells. CD: Cluster of differentiation; FATPs: Fatty acid transport proteins; FABPs: Fatty acid-binding protein; LDLR: Low-density lipoprotein receptor; DAG: Diacylglycerol; DGAT: Diacylglycerol acyltransferase; LD: Lipid droplet; PI3K: Phosphatidylinositol 3-kinase; AKT: Protein kinase B; TGF: Transforming growth factor; TAG: Triacylglycerol; SREBP: Sterol regulatory element-binding protein; PPAR: Peroxisome proliferator-activated receptor; HIF: Hypoxia inducible factor; FASN: Fatty acid synthase; ACSL: Acyl-CoA synthetase long chain; HMGCR: 3-hydroxy-3-methylglutaryl-CoA reductase.