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The metabolic landscape of RAS-driven cancers from biology to therapy
Open accessAbstract
Our understanding of how the RAS protein family, and in particular mutant KRAS, promotes metabolic dysregulation in cancer cells has advanced substantially over the last decade. In this Review, we discuss the metabolic reprogramming mediated by oncogenic RAS in cancer and elucidate the underlying mechanisms that could translate to novel therapeutic opportunities to target metabolic vulnerabilities in RAS-driven cancers. Mukhopadhyay, Vander Heiden and McCormick review the metabolic landscape of RAS-driven cancers, the effects of RAS-directed metabolic reprogramming and opportunities for targeting these cancers therapeutically.
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TL;DR
This review argues that oncogenic RAS, especially mutant KRAS, rewires glucose, glutamine, lipid, redox, and nutrient-scavenging metabolism to support tumor growth and therapy resistance. It surveys preclinical and early clinical strategies for exploiting these metabolic dependencies, while stressing that effective treatments will likely need to be context-specific and combinatorial.
Key findings
- RAS mutations contribute to roughly one third of human cancers, with KRAS predominant in many adenocarcinomas, NRAS prominent in melanoma and myeloid cancers, and HRAS mutated less often but mainly in bladder and head/neck squamous carcinoma. Mutation patterns vary by tissue: about 22% of oncogenic lung adenocarcinoma mutations are KRAS, while nearly 24% of skin cutaneous melanoma mutations are NRAS; G12C dominates in lung adenocarcinoma and G12D in pancreatic adenocarcinoma.
- Mutant KRAS increases glucose uptake and glycolytic flux through GLUT1, HK1/HK2, PFK1, ENO1, and LDHA, and also supports the hexosamine biosynthesis pathway and non-oxidative pentose phosphate pathway. KRAS4A can directly regulate HK1. Proposed glycolytic vulnerabilities include GAPDH inhibition by vitamin C, methylglyoxal scavengers combined with AKT inhibitors, and GLUT inhibitors such as silybin and BAY-876.
- KRAS-driven tumors often depend on glutaminolysis, the GOT1/2–ME1 pathway, NRF2-driven antioxidant programs, and xCT/cysteine metabolism; glutaminase inhibition may be especially relevant in tumors with KEAP1 or LKB1 co-mutations, and cysteine depletion can trigger ferroptosis. Lipid-related targets include ACLY, ACSL3, FASN, and fatty acid oxidation, while nutrient scavenging involves autophagy, NIX-mediated mitophagy, and macropinocytosis, with allele-specific differences such as KRAS G12R being impaired in PI3K signaling and macropinocytosis.
- Therapy resistance is linked to ROS management, stress granule formation via 15-d-PGJ2/NRF2, and compensatory signaling. KRAS G12C inhibitors show promise, but resistance suggests combinations with mTOR, SHP2, CDK4/6, or metabolic inhibitors; clinical trials are targeting glutaminolysis and autophagy.
Methods
- Narrative review, not a primary experimental study; it synthesizes literature on RAS biology and cancer metabolism, focusing mainly on KRAS and noting other isoforms where known.
- Mutation data for figures were compiled from AACR Genie Release 6.1-public, COSMIC v90, cBioPortal, TCGA, and NCI GDC; Figure 4 used previously published driver mutation data from ICGC/TCGA controlled access and an in-house pathway pattern extraction pipeline implemented in R.
- No systematic review, meta-analysis, or new experimental data are reported.
Limitations
- The authors state that many open questions remain: the interplay among KRAS isoforms, RAS alleles, tissue of origin, and metabolic alterations is poorly understood; whether RAS-mediated metabolic changes are common across all RAS-driven cancers is unanswered; and HRAS/NRAS metabolic landscapes are less explored.
- The authors note that metabolic flexibility and compensatory pathways can limit single-pathway targeting, that toxicity to normal cells and immune cells is a major concern, and that in vivo glutamine dependencies can differ from cell-culture findings, making model choice important.
- Evident from the text: as a review, it provides no primary validation or systematic search criteria, and many proposed metabolic therapies remain preclinical or early clinical and unapproved.
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52 Not checked yet · 2 Own interpretation · 1 Supported · 1 Partly supported · accuracy not yet measured
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In the paper
“Moreover, glycolytic KRAS-mutant cells produce increased amounts of potentially toxic byproducts of glycolysis such as methylglyoxal40.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Interplay between oncogenic RAS and glucose metabolism
What the sources say
- Supportedcites [40] Bellier, J. et al. Methylglyoxal scavengers resensitize KRAS-mutated colorectal tumors to cetuximab. Cell Rep 30, 1400–1416 e1406 (2020). source
The Results section (p. 5) reports higher methylglyoxal levels in glycolytic KRAS G12V colorectal cancer cells than in isogenic KRAS wild-type cells. It also identifies methylglyoxal as a glycolysis byproduct using labeled-glucose experiments. (LLM, conf=0.94)
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In the paper
“This could be explained by the fact that loss of LKB1 sustains KRAS-mediated proliferation through autophagy and increased synthesis of essential macromolecules, even under nutrient-deprived conditions68.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Oncogenic RAS in glutaminolysis and redox homeostasis
What the sources say
- Partly supportedcites [68] Faubert, B., Solmonson, A. & DeBerardinis, R. J. Metabolic reprogramming and cancer progression. Science https://doi.org/10.1126/science.aaw5473 (2020). sourceExperimental — accuracy not yet measured
The Primary invasive cancers section (page not provided) says that LKB1 normally restrains anabolism during energetic stress and that combined KRAS–STK11 mutations are associated with aggressive tumors and altered metabolism. It also discusses continued proliferation under nutrient deprivation, but does not link that outcome specifically to LKB1 loss through autophagy and increased macromolecule synthesis. (LLM, conf=0.86)
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In the paper
“Analysis of data from the PanCancer Analysis of Whole Genomes Consortium samples135 on the KEGG pathway database137 depicts oncogenic driver genes involved in various metabolism processes in many cancer tissue types (Fig. 4a)”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > Targeting oncogenic RAS-related metabolism > Connecting RAS to other oncogenic drivers and metabolic pathways
What the sources say
- Not checked yetcites [135] ICGC/TCGA Pan-Cancer Analysis of Whole Genomes Consortium. Pan-cancer analysis of whole genomes. Nature 578, 82–93 (2020). source
- Not checked yetcites [137] Alam, H. et al. KMT2D deficiency impairs super-enhancers to confer a glycolytic vulnerability in lung cancer. Cancer Cell 37, 599–617 (2020). source
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In the paper
“with a gene-level analysis of each corresponding pathway unveiling driver genes that are co-altered in diverse tissue types (Fig. 4b).”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > Targeting oncogenic RAS-related metabolism > Connecting RAS to other oncogenic drivers and metabolic pathways
What the sources say
- Not checked yetcites [135] ICGC/TCGA Pan-Cancer Analysis of Whole Genomes Consortium. Pan-cancer analysis of whole genomes. Nature 578, 82–93 (2020). source
- Not checked yetcites [137] Alam, H. et al. KMT2D deficiency impairs super-enhancers to confer a glycolytic vulnerability in lung cancer. Cancer Cell 37, 599–617 (2020). source
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In the paper
“Network analysis of the several driver mutation genes, including KMT2D138, PIK3CA139, PTEN140, and IDH1141, that regulate signaling and metabolic pathways in KRAS-driven cancers, connects them to oncogenic RAS (Fig 4c).”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > Targeting oncogenic RAS-related metabolism > Connecting RAS to other oncogenic drivers and metabolic pathways
What the sources say
- Not checked yetcites [138] Castellano, E. & Downward, J. RAS interaction with PI3K: more than just another effector pathway. Genes Cancer 2, 261–274 (2011). source
- Not checked yetcites [139] Nogueira, C. et al. Cooperative interactions of PTEN deficiency and RAS activation in melanoma metastasis. Oncogene 29, 6222–6232 (2010). source
- Not checked yetcites [140] Wakimoto, H. et al. Targetable signaling pathway mutations are associated with malignant phenotype in IDH-mutant gliomas. Clin. Cancer Res. 20, 2898–2909 (2014). source
- Not checked yetcites [141] Fernandez-Garcia, B. et al. p73 cooperates with Ras in the activation of MAP kinase signaling cascade. Cell Death Differ. 14, 254–265 (2007). source
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In the paper
“When mutated, oncogenic RAS remains preferentially in the active GTP-bound state, whereas GTP hydrolysis by its GTPase function and enzymes such as GTPase-activating proteins, is compromised1,2.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > Introduction
What the sources say
- Not checked yetcites [1] Simanshu, D. K., Nissley, D. V. & McCormick, F. RAS proteins and their regulators in human disease. Cell 170, 17–33 (2017). source
- Not checked yetcites [2] Stalnecker, C. A. & Der, C. J. RAS, wanted dead or alive: advances in targeting RAS mutant cancers. Sci. Signal. https://doi.org/10.1126/scisignal.aay6013 (2020). source
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In the paper
“KRAS also promotes the hexosamine biosynthesis pathway (HBP), which provides precursors for lipid and protein glycosylation34, and the non-oxidative arm of the pentose phosphate pathway (PPP)28, which supplies ribose, the backbone for nucleic acid production35 (Fig 2).”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Interplay between oncogenic RAS and glucose metabolism
What the sources say
- Not checked yetcites [34] Slawson, C., Copeland, R. J. & Hart, G. W. O-GlcNAc signaling: a metabolic link between diabetes and cancer? Trends Biochem. Sci. 35, 547–555 (2010). source
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In the paper
“The breakdown of glutamine through glutaminolysis gives rise to glutamate, a critical precursor of most other nonessential amino acids, including aspartate, alanine, arginine, and proline52.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Oncogenic RAS in glutaminolysis and redox homeostasis
What the sources say
- Not checked yetcites [52] Yang, L., Venneti, S. & Nagrath, D. Glutaminolysis: a hallmark of cancer metabolism. Annu. Rev. Biomed. Eng. 19, 163–194 (2017). source
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In the paper
“The resulting RAS-mediated signaling cascades drive tumor initiation, maintenance and progression by deregulating key cellular processes, for instance by increasing proliferation and suppressing apoptosis, but also by rewiring cellular metabolism and promoting alterations in the tumor microenvironment3.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > Introduction
What the sources say
- Not checked yetcites [3] Pylayeva-Gupta, Y., Grabocka, E. & Bar-Sagi, D. RAS oncogenes: weaving a tumorigenic web. Nat. Rev. Cancer 11, 761–774 (2011). source
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In the paper
“These observations indicate a fundamental difference in the biological effects of specific mutations on different RAS isoforms and in different tissues.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS mutations in cancer
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In the paper
“KRAS in particular, is among the most frequently mutated oncogenes in cancer and is commonly associated with therapeutic resistance and poor prognosis1,5,6.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > Introduction
What the sources say
- Not checked yetcites [1] Simanshu, D. K., Nissley, D. V. & McCormick, F. RAS proteins and their regulators in human disease. Cell 170, 17–33 (2017). source
- Not checked yetcites [5] Vogelstein, B. et al. Cancer genome landscapes. Science 339, 1546–1558 (2013). source
- Not checked yetcites [6] Haigis, K. M. KRAS alleles: the devil is in the detail. Trends Cancer 3, 686–697 (2017). source
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In the paper
“Furthermore, the tumor suppressor LKB1, which activates the energy sensor and metabolic regulator AMPK, has been linked to serine metabolism and induction of tumorigenesis45.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Interplay between oncogenic RAS and glucose metabolism
What the sources say
- Not checked yetcites [45] Kottakis, F. et al. LKB1 loss links serine metabolism to DNA methylation and tumorigenesis. Nature 539, 390–395 (2016). source
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In the paper
“However, the initial enthusiasm has been somewhat tempered by work suggesting that acquired resistance may constrain the inhibitors’ efficacy, which indicates that combination therapies may be needed11–14.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > Introduction
What the sources say
- Not checked yetcites [11] Hata, A. N. & Shaw, A. T. Resistance looms for KRASG12C inhibitors. Nat. Med. 26, 169–170 (2020). source
- Not checked yetcites [12] Bar-Sagi, D., Knelson, E. H. & Sequist, L. V. A bright future for KRAS inhibitors. Nat. Cancer 1, 25–27 (2020). source
- Not checked yetcites [13] Fedele, C. et al. SHP2 inhibition diminishes KRASG12C cycling and promotes tumor microenvironment remodeling. J. Exp. Med. https://doi.org/10.1084/jem.20201414 (2021). source
- Not checked yetcites [14] Ryan, M. B. et al. Vertical pathway inhibition overcomes adaptive feedback resistance to KRASG12C inhibition. Clin. Cancer Res. 26, 1633–1643 (2020). source
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In the paper
“Additionally, oncogenic HRAS mediates enhanced glycolytic rates including increased glucose uptake, underscoring the fact that increased aerobic glycolysis is essential for RAS-mutant tumors to match energy production with the requirement for enhanced biosynthetic pathways39.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Interplay between oncogenic RAS and glucose metabolism
What the sources say
- Not checked yetcites [39] Lock, R. et al. Autophagy facilitates glycolysis during Ras-mediated oncogenic transformation. Mol. Biol. Cell 22, 165–178 (2011). source
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In the paper
“The recognition that oncogenes, including RAS, can promote aerobic glycolysis, commonly known as the Warburg effect, and activate anabolic pathways 22,23, has increased efforts to understand the molecular underpinnings of altered metabolism in cancer24.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism
What the sources say
- Not checked yetcites [22] Nagarajan, A., Malvi, P. & Wajapeyee, N. Oncogene-directed alterations in cancer cell metabolism. Trends Cancer 2, 365–377 (2016). source
- Not checked yetcites [23] Levine, A. J. & Puzio-Kuter, A. M. The control of the metabolic switch in cancers by oncogenes and tumor suppressor genes. Science 330, 1340–1344 (2010). source
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In the paper
“A promising candidate is silybin, a natural flavonoid and potent inhibitor of GLUT1 and GLUT4, which was shown to be effective in phase 1 trial of prostate cancer with asymptotic liver toxicity as an adverse effect48.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Interplay between oncogenic RAS and glucose metabolism
What the sources say
- Not checked yetcites [48] Flaig, T. W. et al. A phase I and pharmacokinetic study of silybin-phytosome in prostate cancer patients. Invest. New Drugs 25, 139–146 (2007). source
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In the paper
“Oncogenic KRAS also upregulates expression of other key glycolytic enzymes, such as PFK1, ENO1, and LDHA28,31–33, thereby promoting glycolytic flux and enabling the production of glycolytic intermediates that can be shunted into other anabolic pathways (Fig 2).”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Interplay between oncogenic RAS and glucose metabolism
What the sources say
- Not checked yetcites [28] Ying, H. et al. Oncogenic Kras maintains pancreatic tumors through regulation of anabolic glucose metabolism. Cell 149, 656–670 (2012). source
- Not checked yetcites [31] Kole, H. K., Resnick, R. J., Van Doren, M. & Racker, E. Regulation of 6-phosphofructo-1-kinase activity in ras-transformed rat-1 fibroblasts. Arch. Biochem. Biophys. 286, 586–590 (1991). source
- Not checked yetcites [32] Racker, E., Resnick, R. J. & Feldman, R. Glycolysis and methylaminoisobutyrate uptake in rat-1 cells transfected with ras or myc oncogenes. Proc. Natl Acad. Sci. USA 82, 3535–3538 (1985). source
- Not checked yetcites [33] Chun, S. Y. et al. Oncogenic KRAS modulates mitochondrial metabolism in human colon cancer cells by inducing HIF-1α and HIF-2α target genes. Mol. Cancer 9, 293 (2010). source
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In the paper
“Of note, LKB1 loss is prevalent in KRAS mutant lung cancers46, indicating that oncogenic KRAS not only induces mTOR activity, but might also upregulate one-carbon metabolism by undermining AMPK’s inhibitory role in the folate cycle.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Interplay between oncogenic RAS and glucose metabolism
What the sources say
- Not checked yetcites [46] Calles, A. et al. Immunohistochemical loss of LKB1 is a biomarker for more aggressive biology in KRAS-mutant lung adenocarcinoma. Clin. Cancer Res. 21, 2851–2860 (2015). source
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In the paper
“Mutant KRAS has also been implicated in the induction of enzymes involved in the folate cycle42 and the aberrant activation of mTOR, a key regulator for both serine synthesis and the folate cycle43,44.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Interplay between oncogenic RAS and glucose metabolism
What the sources say
- Not checked yetcites [42] Moran, D. M. et al. KRAS mutation status is associated with enhanced dependency on folate metabolism pathways in non-small cell lung cancer cells. Mol. Cancer Ther. 13, 1611–1624 (2014). source
- Not checked yetcites [43] Gomes, A. P. & Blenis, J. A nexus for cellular homeostasis: the interplay between metabolic and signal transduction pathways. Curr. Opin. Biotechnol. 34, 110–117 (2015). source
- Not checked yetcites [44] Ben-Sahra, I., Hoxhaj, G., Ricoult, S. J. H., Asara, J. M. & Manning, B. D. mTORC1 induces purine synthesis through control of the mitochondrial tetrahydrofolate cycle. Science 351, 728–733 (2016). source
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In the paper
“Overall, KRAS is mutated in many cancers (predominantly adenocarcinomas), whereas NRAS mutations are prominent in melanoma and myeloid cancer4,15,16 (Fig. 1).”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS mutations in cancer
What the sources say
- Not checked yetcites [4] Prior, I. A., Lewis, P. D. & Mattos, C. A comprehensive survey of Ras mutations in cancer. Cancer Res. 72, 2457–2467 (2012). source
- Not checked yetcites [15] Prior, I. A., Hood, F. E. & Hartley, J. L. The frequency of Ras mutations in cancer. Cancer Res. 80, 2969–2974 (2020). source
- Not checked yetcites [16] Moore, A. R., Rosenberg, S. C., McCormick, F. & Malek, S. RAS-targeted therapies: is the undruggable drugged? Nat. Rev. Drug Discov. 19, 533–552 (2020). source
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In the paper
“Consequently, treatment efficacy cannot be extrapolated from one RAS-driven cancer to another, but rather therapeutic approaches must be tailored to the isoform, mutation and tissue.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS mutations in cancer
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In the paper
“For instance, 22% of oncogenic mutations in lung adenocarcinoma (LUAD) occur in KRAS, whereas nearly 24% of such mutations in skin cutaneous melanoma occur in NRAS15 (Fig. 1b).”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS mutations in cancer
What the sources say
- Not checked yetcites [15] Prior, I. A., Hood, F. E. & Hartley, J. L. The frequency of Ras mutations in cancer. Cancer Res. 80, 2969–2974 (2020). source
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In the paper
“Highly glycolytic RAS-mutant cells have been found to be vulnerable to inhibition of the glycolytic enzymes glyceraldehyde 3-phosphate dehydrogenase (GAPDH) with Vitamin C, providing a mechanistic rationale for exploring the therapeutic use of this vitamin against KRAS or BRAF mutant colorectal cancer preclinical models 38.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Interplay between oncogenic RAS and glucose metabolism
What the sources say
- Not checked yetcites [38] Yun, J. et al. Vitamin C selectively kills KRAS and BRAF mutant colorectal cancer cells by targeting GAPDH. Science 350, 1391–1396 (2015). source
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In the paper
“However, RAS mutations and the resulting deregulated signaling events are responsible for one third of all human cancers4 (Figure 1).”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > Introduction
What the sources say
- Not checked yetcites [4] Prior, I. A., Lewis, P. D. & Mattos, C. A comprehensive survey of Ras mutations in cancer. Cancer Res. 72, 2457–2467 (2012). source
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In the paper
“Gene expression and metabolic flux analyses have shown that it upregulates the expression of the GLUT1 glucose transporter to promote glucose uptake by cells, as well as inducing expression of hexokinase 1 and 2 (HK1 and HK2) rate-limiting enzymes of glycolysis, to increase glycolytic activity27–30 (Fig. 2a).”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Interplay between oncogenic RAS and glucose metabolism
What the sources say
- Not checked yetcites [27] Gaglio, D. et al. Oncogenic K-Ras decouples glucose and glutamine metabolism to support cancer cell growth. Mol. Syst. Biol. 7, 523 (2011). source
- Not checked yetcites [28] Ying, H. et al. Oncogenic Kras maintains pancreatic tumors through regulation of anabolic glucose metabolism. Cell 149, 656–670 (2012). source
- Not checked yetcites [29] Amendola, C. R. et al. KRAS4A directly regulates hexokinase 1. Nature 576, 482–486 (2019). source
- Not checked yetcites [30] Yun, J. et al. Glucose deprivation contributes to the development of KRAS pathway mutations in tumor cells. Science 325, 1555–1559 (2009). source
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In the paper
“Methylglyoxal-mediated stress was shown to be involved in cancer progression41 and to be a potent activator of AKT signaling, suggesting that utilizing methylglyoxal scavengers in KRAS mutant colorectal cancer cells might be more effective when combined with AKT inhibitors40.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Interplay between oncogenic RAS and glucose metabolism
What the sources say
- Not checked yetcites [40] Bellier, J. et al. Methylglyoxal scavengers resensitize KRAS-mutated colorectal tumors to cetuximab. Cell Rep 30, 1400–1416 e1406 (2020). source
- Not checked yetcites [41] Bellahcene, A., Nokin, M. J., Castronovo, V. & Schalkwijk, C. Methylglyoxal-derived stress: an emerging biological factor involved in the onset and progression of cancer. Semin. Cancer Biol. 49, 64–74 (2018). source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“KRAS regulates these pathways through MAPK-dependent signaling cascades, ultimately supporting cell survival and conferring a proliferative advantage on tumors28,36,37.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Interplay between oncogenic RAS and glucose metabolism
What the sources say
- Not checked yetcites [28] Ying, H. et al. Oncogenic Kras maintains pancreatic tumors through regulation of anabolic glucose metabolism. Cell 149, 656–670 (2012). source
- Not checked yetcites [36] Taparra, K. et al. O-GlcNAcylation is required for mutant KRAS-induced lung tumorigenesis. J. Clin. Invest. 128, 4924–4937 (2018). source
- Not checked yetcites [37] Santana-Codina, N. et al. Oncogenic KRAS supports pancreatic cancer through regulation of nucleotide synthesis. Nat. Commun. 9, 4945 (2018). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Limiting glutamine use combined with chemotherapy is a viable means to halt pancreatic tumor growth in preclinical mouse models and is not toxic to normal cells58,60,65.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Oncogenic RAS in glutaminolysis and redox homeostasis
What the sources say
- Not checked yetcites [58] Mukhopadhyay, S., Saqcena, M. & Foster, D. A. Synthetic lethality in KRas-driven cancer cells created by glutamine deprivation. Oncoscience 2, 807–808 (2015). source
- Not checked yetcites [60] Mukhopadhyay, S. et al. Undermining glutaminolysis bolsters chemotherapy while NRF2 promotes chemoresistance in KRAS-driven pancreatic cancers. Cancer Res. https://doi.org/10.1158/0008-5472.CAN-19-1363 (2020). source
- Not checked yetcites [65] Saqcena, M. et al. Blocking anaplerotic entry of glutamine into the TCA cycle sensitizes K-Ras mutant cancer cells to cytotoxic drugs. Oncogene 34, 2672–2680 (2015). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Cells from advanced lung tumors with oncogenic KRAS and loss-of-function KEAP1 mutations were more dependent on increased amounts of glutamine than other cells, making them more susceptible to glutaminase inhibition62.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Oncogenic RAS in glutaminolysis and redox homeostasis
What the sources say
- Not checked yetcites [62] Romero, R. et al. Keap1 loss promotes Kras-driven lung cancer and results in dependence on glutaminolysis. Nat. Med. 23, 1362–1368 (2017). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In addition to activating the GOT2/GOT1/Malic Enzyme 1 (ME1) pathway, oncogenic KRAS activates the NRF2 antioxidant system by inducing NRF2 expression59,60 and by constitutively activating the battery of genes controlled by NRF2 to maintain the redox balance and promote tumorigenesis61.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Oncogenic RAS in glutaminolysis and redox homeostasis
What the sources say
- Not checked yetcites [59] DeNicola, G. M. et al. Oncogene-induced Nrf2 transcription promotes ROS detoxification and tumorigenesis. Nature 475, 106–109 (2011). source
- Not checked yetcites [60] Mukhopadhyay, S. et al. Undermining glutaminolysis bolsters chemotherapy while NRF2 promotes chemoresistance in KRAS-driven pancreatic cancers. Cancer Res. https://doi.org/10.1158/0008-5472.CAN-19-1363 (2020). source
- Not checked yetcites [61] Chio, I. I. C. et al. NRF2 promotes tumor maintenance by modulating mRNA translation in pancreatic cancer. Cell 166, 963–976 (2016). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Moreover, KRAS-driven lung adenocarcinomas with TP53 mutation induce immune cell production, while tumors with KEAP1 mutations rewire metabolism71.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Oncogenic RAS in glutaminolysis and redox homeostasis
What the sources say
- Not checked yetcites [71] Best, S. A. et al. Distinct initiating events underpin the immune and metabolic heterogeneity of KRAS-mutant lung adenocarcinoma. Nat. Commun. 10, 4190 (2019). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Concurrent mutations in KRAS and LKB1 also confer vulnerabilities in pancreatic cancer, but the mechanisms are different from those in lung cancer45.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Oncogenic RAS in glutaminolysis and redox homeostasis
What the sources say
- Not checked yetcites [45] Kottakis, F. et al. LKB1 loss links serine metabolism to DNA methylation and tumorigenesis. Nature 539, 390–395 (2016). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Co-occurrence of mutant KRAS and LKB1 deficiency in patients with lung cancer resulted in more aggressive tumors, higher frequency of metastasis, and therapy resistance67.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Oncogenic RAS in glutaminolysis and redox homeostasis
What the sources say
- Not checked yetcites [67] Skoulidis, F. & Heymach, J. V. Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy. Nat. Rev. Cancer 19, 495–509 (2019). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“However, KRAS has also been shown to promote cancer cell growth by stimulating alanine aminotransferase activity, leading to high levels of α-ketoglutarate for the TCA cycle and mitochondrial ROS generation, which was required for mutant KRAS-driven tumorigenesis in a mouse model of lung cancer64.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Oncogenic RAS in glutaminolysis and redox homeostasis
What the sources say
- Not checked yetcites [64] Weinberg, F. et al. Mitochondrial metabolism and ROS generation are essential for Kras-mediated tumorigenicity. Proc. Natl Acad. Sci. USA 107, 8788–8793 (2010). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Several oncogenes coordinate the transcriptional reprogramming that tumor cells need to thrive, with many cancer driver genes also perturbing metabolism135,136.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > Targeting oncogenic RAS-related metabolism > Connecting RAS to other oncogenic drivers and metabolic pathways
What the sources say
- Not checked yetcites [135] ICGC/TCGA Pan-Cancer Analysis of Whole Genomes Consortium. Pan-cancer analysis of whole genomes. Nature 578, 82–93 (2020). source
- Not checked yetcites [136] Kanehisa, M., Goto, S., Furumichi, M., Tanabe, M. & Hirakawa, M. KEGG for representation and analysis of molecular networks involving diseases and drugs. Nucleic Acids Res. 38, D355–D360 (2010). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“For instance, KRAS-dependent upregulation of Glutamate Oxaloacetate Transaminase 1,2. (GOT) expression in pancreatic cancer facilitates production of aspartate for nucleotide biosynthesis, and allows NADPH generation via ME157,58 (Fig 2).”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Oncogenic RAS in glutaminolysis and redox homeostasis
What the sources say
- Not checked yetcites [57] Son, J. et al. Glutamine supports pancreatic cancer growth through a KRAS-regulated metabolic pathway. Nature 496, 101–105 (2013). source
- Not checked yetcites [58] Mukhopadhyay, S., Saqcena, M. & Foster, D. A. Synthetic lethality in KRas-driven cancer cells created by glutamine deprivation. Oncoscience 2, 807–808 (2015). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Moreover, in oncogenic-KRAS-driven lung adenocarcinoma, loss of LKB1 often induces KEAP1 activation69 and leads to metabolic alterations that could be counteracted by activation of NRF270, thereby maintaining redox homeostasis and fueling energy metabolism in a glutamine-dependent manner.”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Oncogenic RAS in glutaminolysis and redox homeostasis
What the sources say
- Not checked yetcites [69] Kaufman, J. M. et al. LKB1 loss induces characteristic patterns of gene expression in human tumors associated with NRF2 activation and attenuation of PI3K–AKT. J. Thorac. Oncol. 9, 794–804 (2014). source
- Not checked yetcites [70] Li, F. et al. LKB1 inactivation elicits a redox imbalance to modulate non-small cell lung cancer plasticity and therapeutic response. Cancer Cell 27, 698–711 (2015). source
hedgeddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper relies on this without support.
Metabolic changes caused by oncogenes can be broad, with several pathways altered at once within one cancer type.
“Oncogene-directed metabolic alterations can have extensive impact, with multiple metabolic pathways being altered simultaneously in a single cancer type.”
The paper relies on this without support.
Metabolic phenotypes differ between tumor types and also vary among tumors of the same type.
“The elucidation of these events should also take into account the fact that metabolic phenotype is not uniform across different tumor types, and variability also exists between different tumors of the same type.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“For example, glutaminase inhibitors and agents targeting aspartate metabolism, such as ASS1 inhibitors, may enhance the efficacy of KRAS inhibitors in colorectal cancer [33,35].”
From The Role of KRAS Mutations in Colorectal Cancer: Biological Insights, Clinical Implications, and Future Therapeutic Perspectives (2025) · cites this paper as [33]
Experimental — accuracy not yet measuredIn the citing paper
“STK11 is also a critical regulator of metabolism via its substrate AMPK (73).”
From Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRASG12C Inhibitor Efficacy (2023) · cites this paper as [73]
In the citing paper
“Oncogenic KRAS significantly reprograms cellular metabolism, enhancing glycolysis, glutaminolysis, and aspartate metabolism to fuel tumor growth and survival.”
From The Role of KRAS Mutations in Colorectal Cancer: Biological Insights, Clinical Implications, and Future Therapeutic Perspectives (2025) · cites this paper as [33]
In the citing paper
“KRAS mutations drive the upregulation of key enzymes, such as PCK1, PCK2, and ASS1, which are involved in aspartate and urea cycle metabolism, contributing to the metabolic flexibility of KRAS-mutant CRC cells [33,34,35].”
From The Role of KRAS Mutations in Colorectal Cancer: Biological Insights, Clinical Implications, and Future Therapeutic Perspectives (2025) · cites this paper as [33]
In the citing paper
“Targeting these pathways has shown promise in preclinical studies.”
From The Role of KRAS Mutations in Colorectal Cancer: Biological Insights, Clinical Implications, and Future Therapeutic Perspectives (2025) · cites this paper as [33]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Oncogenic RAS in glutaminolysis and redox homeostasis
“xCT, the cystine/glutamate antiporter that exports glutamate to the extracellular space and imports cysteine into the cytosol for the production of the amino acid cysteine”
§ The Metabolic Landscape of RAS-Driven Cancers from biology to therapy > RAS and tumor metabolism > Oncogenic RAS in glutaminolysis and redox homeostasis
“Cystine import is key to KRAS-driven PDAC cell survival”
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Metadata
- Authors
- Mukhopadhyay, S., Vander Heiden, M. G., & McCormick, F.
- Affiliations
- NYU Langone Health (US)
- University of California, San Francisco (US)
- Corresponding author
- McCormick, Frank
- Venue
- Nature Cancer
- Published
- 2021-03-24
- Volume
- 2
- Issue
- 3
- Pages
- 271-283
- ISSN
- 2662-1347 (ISSN-L)
- PMC
- PMC8045781
- OpenAlex
- W3138007187
- Semantic Scholar
- 8d6bdc24577b7bfea70417686ccb3aa45bcc6c18
- Cited by
- 315
- References
- 158
- Citations by year
- 2026: 27 · 2025: 48 · 2024: 81 · 2023: 73 · 2022: 56 · 2021: 30
- FWCI
- 7.58
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature Cancer (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by-nc-sa)
- Funders
- Frederick National Laboratory for Cancer Research (HHSN261200800001E)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- RAS-driven cancers, KRAS mutation, oncogenic Ras, tumor metabolic reprogramming, cancer metabolism, metabolic vulnerability, metabolic cancer therapy, Ras signaling
- MeSH terms
- Biology, Humans, Neoplasms, Genes, ras, ras Proteins
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