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. 2021 Jul 5;6:249. doi: 10.1038/s41392-021-00659-4

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Metabolic reprogramming in pancreatic cancer cells. KRAS activation and mutant TP53 enhance glucose metabolism to provide biosynthetic precursors for anabolic pathways, including the non-oxidative arm of the pentose phosphate pathway (PPP) and the hexosamine biosynthesis pathway (HBP). KRAS activation reprograms glutamine metabolism to sustain cellular redox homeostasis by increasing the NADPH/NADP⁺ ratio and recycling glutathione (GSH) via reduction of oxidized GSH. The BCAT2-mediated BCAA catabolism driven by KRAS plays a critical role during pancreatic cancer development. Enhanced nutrient salvaging, via the induction of macropinocytosis and autophagy, provides energy and regenerative nutrients, including glucose, amino acids, lipids, and nucleosides