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. Author manuscript; available in PMC: 2014 Feb 1.
Published in final edited form as: Trends Mol Med. 2012 Dec 5;19(2):74–82. doi: 10.1016/j.molmed.2012.10.011

Figure 1.

Figure 1

Cancer cells undergo metabolic re-programming. The glycolytic pathway in normal cells (a) is used to generate pyruvate that enters the citric acid (TCA) cycle in the mitochondria. In cancer cells (b), many of the enzymes of the glycolytic pathway are upregulated and/or activated, although M2 pyruvate kinase activity, which catalyzes the penultimate step in the pathway, is inhibited by tyrosine phosphorylation. Pyruvate produced by PKM2 is preferentially converted to lactate (as catalyzed by lactate dehydrogenase). Elevated glutamine metabolism, through the up-regulation and/or activation of GAC (which converts glutamine to glutamate) and GDH (converting glutamate to α-ketoglutarate), is then essential for ‘feeding’ the TCA cycle in cancer cells. Abbreviations: Glut1, glucose transporter 1; HK, hexokinase; PEP, phosphoenolpyruvate; PKM, pyruvate kinase M; LDH, lactate dehydrogenase; PDH, pyruvate dehydrogenase; AcCoA, acetyl CoA; PTK, protein tyrosine kinase; GAC, glutaminase C; GDH, glutamate dehydrogenase; αKG, α-ketoglutarate. Dashed lines represent multistep pathways; heavy lines represent preferred and/or accelerated pathways.