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. Author manuscript; available in PMC: 2017 Jun 5.
Published in final edited form as: Curr Opin Genet Dev. 2016 Jun 5;38:102–109. doi: 10.1016/j.gde.2016.05.003

Figure 2.

Figure 2

Metabolic reprogramming alters pyruvate metabolism in some cancers: A) Dimeric PKM2 prevents the glycolytic production of pyruvate. Pyruvate is shunted away from mitochondrial metabolism by reduction to lactate. B) Citrate produced by the TCA cycle is converted to acetyl-CoA in the cytoplasm for de novo lipogenesis. Acetyl-CoA may also be generated directly from acetate by acetyl-CoA synthetase 2. C) In the absence of MPC activity in highly oxidative cancers glutaminolysis maintains TCA cycle intermediate pools. When MPC activity is decreased, reductive carboxylation of α-ketoglutarate supports citrate production for de novo lipogenesis. D) Some cancers rely on pyruvate carboxylase to produce oxaloacetate. Oxaloacetate may be transaminated to aspartate to support protein synthesis.