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. Author manuscript; available in PMC: 2016 Jul 11.
Published in final edited form as: Nat Cell Biol. 2015 Mar 16;17(4):351–359. doi: 10.1038/ncb3124

Figure 2.

Figure 2

Catabolic pathways support metabolism during nutrient stress. Under conditions of nutrient deprivation and other stresses, tumorigenic mutations also reprogram metabolism to support cell survival. In particular, KRas stimulates autophagy and macropinocytosis and facilitates fatty acid uptake. Mutations in BRaf also lead to enhanced autophagy. p53 promotes NADPH production through the pentose phosphate pathway to maintain redox homeostasis. Acetate and branched-chain amino acids serve as alternative substrates to support metabolism. Oncogenic drivers are highlighted in green, while tumour suppressors are shown in red. Important metabolic enzymes are highlighted in blue. Classic cancer metabolic pathways are shown in orange, while emerging pathways and activities supporting cell proliferation are shown in purple. G6P, glucose-6-phosphate; PPP, pentose phosphate pathway; ribose-5P, ribose-5-phosphate; F6P, fructose-6-phosphate; TCA, tricarboxylic acid; α-KG, alpha-ketoglutarate; OAA, oxaloacetate; BCAA, branched-chain amino acid; CS, citrate synthase; ME, malic enzyme; ACSS2, acetyl-CoA synthetase 2.