Skip to main content
. Author manuscript; available in PMC: 2017 Jul 21.
Published in final edited form as: Cold Spring Harb Symp Quant Biol. 2017 Feb 16;81:73–78. doi: 10.1101/sqb.2016.81.030981

Figure 2.

Figure 2

Defective autophagy in tumor cells alters metabolic flux from glutamine to aspartate and to de novo nucleotide synthesis. K-ras-driven tumor cells depend on autophagy to supply the substrate glutamine and its derivatives to sustain mitochondria metabolism for starvation survival. To compensate, Atg7-deficient tumor cells significantly increase glutamine flux to the tricarboxylic acid (TCA) cycle, de novo nucleotide synthesis, and nicotinamide adenine dinucleotide phosphate (NADPH) generation by up-regulating flux from malate, pyruvate, acetyl-CoA, and citrate for antioxidant defense (Guo et al. 2016). OAA, oxaloacetate; α-KG, α-ketogluturate.