Metabolic Alteration in Hepatocellular Carcinoma: Mechanism of Lipid Accumulation in Well-Differentiated Hepatocellular Carcinoma

Figure 1

Metabolic gene expression in cancer tissues relative to noncancer tissues in human HCC samples. Quantitative RT-PCR analysis of metabolic genes related to (a) glucose metabolism, (b) pyruvate metabolism, tricarboxylic acid (TCA) cycle, (c) fatty acid (FA) synthesis and uptake, (d) triglyceride (TG) hydrolysis and secretion, and β-oxidation. The gene expression levels of cancer tissues were normalized to those of noncancer tissues and were presented as mean ± SE. and vs. noncancer tissue. GK, glucokinase; G6PD, glucose-6-phosphate dehydrogenase; PK, pyruvate kinase; PEPCK, phosphoenolpyruvate carboxykinase; PDH, pyruvate dehydrogenase; PDK, pyruvate dehydrogenase kinase; ACO, aconitase; IDH, isocitrate dehydrogenase; ACC, acetyl-coenzyme A carboxylase; FAS, fatty acid synthase; SREBP, sterol regulatory element-binding protein; PPAR, peroxisome proliferator-activated receptor; DGAT, diacylglycerol acyltransferase; HSL, hormone-sensitive lipase; MTP, microsomal triglyceride transfer protein; CPT, carnitine palmitoyltransferase; LCAD, long chain acyl-coenzyme A dehydrogenase; HADH, hydroxyacyl-coenzyme A dehydrogenase.

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