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. 2015 Mar 27;7:57–68. doi: 10.2147/CPAA.S79760

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© Chakrabarti et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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KRAS-reprogrammed glutamine metabolism in pancreatic cancer.

Notes: In KRAS-mutant pancreatic cancer, mitochondrial glutamine flux is reprogrammed to predominantly flux through GOT2, instead of the canonical GLUD1 pathway. The Asp produced from this reaction is shuttled to the cytoplasm to produce pyruvate and NADPH from malate via cytosolic ME1. TCA cycle-derived malate can also produce NADPH from mitochondrial ME2. Wild-type p53 inhibits both ME1 and ME2. BPTES and CB-839 are non-competitive small-molecule inhibitors of mitochondrial GLS1.

Abbreviations: GOT2, mitochondrial aspartate transaminase; GLUD1, glutamate dehydrogenase 1; Asp, aspartate; NADPH, nicotinamide adenine dinucleotide phosphate; ME1, malic enzyme 1; ME2, malic enzyme 2; BPTES, bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide 3; GLS1, glutaminase 1; MDH1, malate dehydrogenase 1; GOT1, cytosolic aspartate transaminase; OAA, oxaloacetate; αKG, α-ketoglutarate; TCA, tricarboxylic acid cycle.