Oncogenic KRAS creates an aspartate metabolism signature in colorectal cancer cells
Open accessAbstract
Oncogenic mutations in the KRAS gene are found in 30–50% of colorectal cancers (CRC), and recent findings have demonstrated independent and nonredundant roles for wild‐type and mutant KRAS alleles in governing signaling and metabolism. Here, we quantify proteomic changes manifested by KRAS mutation and KRAS allele loss in isogenic cell lines. We show that the expression of KRAS G13D upregulates aspartate metabolizing proteins including PCK1, PCK2, ASNS, and ASS1. Furthermore, differential expression analyses of transcript‐level data from CRC tumors identified the upregulation of urea cycle enzymes in CRC. We find that expression of ASS1 supports colorectal cancer cell proliferation and promotes tumor formation in vitro . We show that loss of ASS1 can be rescued with high levels of several metabolites.
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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.
“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 [35]
Oncogenic KRAS significantly reprograms cellular metabolism, enhancing glycolysis, glutaminolysis, and aspartate metabolism to fuel tumor growth and survival.
“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 [35]
Targeting KRAS-driven metabolic pathways has shown promise in preclinical studies.
“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 [35]
Glutaminase inhibitors and agents targeting aspartate metabolism, such as ASS1 inhibitors, may enhance the efficacy of KRAS inhibitors in colorectal cancer.
“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 [35]
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- Authors
- Doubleday, P. F., Fornelli, L., Ntai, I., & Kelleher, N. L.
- Affiliations
- Northwestern University (US)
- University of Oklahoma (US)
- Thermo Fisher Scientific (United States) (US)
- Corresponding author
- Kelleher, Neil L.
- Venue
- The FEBS Journal
- Publisher
- Wiley
- Published
- 2021-07-27
- Volume
- 288
- Issue
- 23
- Pages
- 6683-6699
- ISSN
- 1742-464X (ISSN-L)
- 1742-4658
- PMC
- PMC8648997
- OpenAlex
- W3182740681
- Cited by
- 23
- References
- 58
- Citations by year
- 2026: 5 · 2025: 8 · 2024: 3 · 2023: 2 · 2022: 5
- FWCI
- 0.99
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- FEBS Journal (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of General Medical Sciences
- Sherman Fairchild Foundation
- National Cancer Institute
- National Institutes of Health (HHSN261200800001E)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Keywords
- KRAS mutation, colorectal cancer, aspartate metabolism, ASS1, urea cycle, PCK1, PCK2, asparagine synthetase, tumor cell proliferation, isogenic cell lines, proteome changes, cancer metabolism
- MeSH terms
- Argininosuccinate Synthase, Aspartic Acid, Humans, Mutation, Phosphoenolpyruvate Carboxykinase (GTP), Colorectal Neoplasms, Signal Transduction, Gene Expression Regulation, Neoplastic, Proto-Oncogene Proteins p21(ras), Carbon-Nitrogen Ligases with Glutamine as Amide-N-Donor, Phosphoenolpyruvate Carboxykinase (ATP), Gene Expression Profiling, Proteomics, Cell Line, Tumor, Intracellular Signaling Peptides and Proteins, Cell Proliferation, Metabolomics, Carcinogenesis, Gene Ontology
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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