Characterization of metabolic landscape in hepatocellular carcinoma

Figure 2 Two distinct principles governing glutamine metabolism in hepatocellular carcinoma. A: Glutaminolysis in MYC-induced hepatocellular carcinoma (HCC) is enhanced via increasing transport and catabolism to fuel Krebs cycle; B: In HCC bearing β-catenin mutation, glutamine accumulation in response to glutamine synthetase upregulation further activates phosphorylated mammalian target of rapamycin. GLS1: Kidney-type glutaminase; GLS2: Liver type glutaminase; Gln: Glutamine; GS: Glutamine synthetase; SLC1A5: Solute-linked carrier family A1 member 5; p-4EBP1: Phosphorylated 4E-binding protein 1; p-mTOR: Phosphorylated mammalian target of rapamycin.