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. 2019 Dec 18;10(12):955. doi: 10.1038/s41419-019-2192-y

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© The Author(s) 2019

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. 3 — Oncogenic RAS drives multiple antioxidant programs by altering intracellular metabolism, such as by driving GSH and NADPH production via the TCA cycle, by generating NAPDH through an alternative glutamine metabolic pathway mediated by aspartate aminotransferase (GOT1), or potentially by generating NADPH via a fatty acid oxidation pathway mediated by acyl-coenzyme A (CoA) synthetase long-chain family member 3 (ACSL3). In addition, oncogenic RAS upregulates several key antioxidant proteins, including the light-chain subunit of the system x_c⁻ transporter (xCT), nuclear factor, erythroid 2-like 2 (NRF2), and gamma-glutamyltransferase 2 (GGT2).