Characterization of metabolic landscape in hepatocellular carcinoma

Figure 1 Hepatocellular carcinoma develops two distinct lipid metabolism patterns depending on the environment or genetic background of tumor cells. A: In most conditions including hypoxia environment, and steatohepatitic or nonalcoholic steato-hepatitis-driven hepatocellular carcinoma (HCC), β-oxidation is repressed to avoid excessive oxidative damage; B: In HCC harboring β-catenin mutation, β-oxidation is promoted to trigger HCC. CACT: Carnitine–acylcarnitine translocase; CPT1: Carnitine palmitoyltransferase 1; CPT2: Carnitine palmitoyltransferase 2; FA: Fatty acid; HCC: Hepatocellular carcinoma; HIF-1α: Hypoxia inducible factor 1 subunit alpha; LCAD: Long-chain acyl-CoA dehydrogenases; MCAD: Medium-chain acyl-CoA dehydrogenases; MUFA: Monounsaturated fatty acid; PPARα: Peroxisome proliferator activated receptor alpha; SCD: Stearoyl-CoA desaturase.