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Glutaminolysis: A Hallmark of Cancer Metabolism
Open accessAbstract
Glutamine is the most abundant circulating amino acid in blood and muscle and is critical for many fundamental cell functions in cancer cells, including synthesis of metabolites that maintain mitochondrial metabolism; generation of antioxidants to remove reactive oxygen species; synthesis of nonessential amino acids (NEAAs), purines, pyrimidines, and fatty acids for cellular replication; and activation of cell signaling. In light of the pleiotropic role of glutamine in cancer cells, a comprehensive understanding of glutamine metabolism is essential for the development of metabolic therapeutic strategies for targeting cancer cells. In this article, we review oncogene-, tumor suppressor–, and tumor microenvironment–mediated regulation of glutamine metabolism in cancer cells. We describe the mechanism of glutamine's regulation of tumor proliferation, metastasis, and global methylation. Furthermore, we highlight the therapeutic potential of glutamine metabolism and emphasize that clinical application of in vivo assessment of glutamine metabolism is critical for identifying new ways to treat patients through glutamine-based metabolic therapy.
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In the citing 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.”
From The metabolic landscape of RAS-driven cancers from biology to therapy (2021) · cites this paper as [52]
In the citing paper
“Glutamine is also a major source of nitrogen for proliferating cells52,54.”
From The metabolic landscape of RAS-driven cancers from biology to therapy (2021) · cites this paper as [52]
In the citing paper
“In addition to pyruvate-derived acetyl-CoA, α-KG-derived metabolites (e.g., succinate and fumarate) generated via glutaminolysis are considered oncometabolites contributing to tumorigenesis23.”
From Glutamine reliance in cell metabolism (2020) · cites this paper as [23]
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“Mitochondrial α-KG can then participate in the TCA cycle, supporting the oxidative phosphorylation (OXPHOS) pathway or the reductive carboxylation pathway23.”
From Glutamine reliance in cell metabolism (2020) · cites this paper as [23]
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Metadata
- Authors
- Yang, L., Venneti, S., & Nagrath, D.
- Affiliations
- Rice University (US)
- University of Michigan (US)
- Venue
- Annual Review of Biomedical Engineering
- Publisher
- Annual Reviews
- Published
- 2017-06-21
- Volume
- 19
- Issue
- 1
- Pages
- 163-194
- ISSN
- 1523-9829 (ISSN-L)
- 1545-4274
- OpenAlex
- W2534904302
- Cited by
- 859
- References
- 171
- Citations by year
- 2026: 68 · 2025: 140 · 2024: 137 · 2023: 132 · 2022: 126 · 2021: 98 · 2020: 71 · 2019: 46 · 2018: 28 · 2017: 13
- FWCI
- 4.43
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annual Review of Biomedical Engineering (publishedVersion)
- PubMed (publishedVersion)
- Rice Research Repository (Rice University) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biotechnology › Bacterial Cancer Therapy
- Keywords
- glutamine metabolism, glutaminolysis, cancer metabolism, tumor microenvironment, oncogenes, tumor suppressor, metastasis, global DNA methylation, tumor cell proliferation, metabolic therapy, reactive oxygen species, purine and pyrimidine synthesis, signal transduction
- MeSH terms
- Animals, Cell Transformation, Neoplastic, Glutamine, Humans, Mitochondria, Models, Biological, Neoplasms, Biomarkers, Tumor, Signal Transduction, Cell Proliferation
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