From Krebs to clinic: glutamine metabolism to cancer therapy
Open accessAbstract
The resurgence of research into cancer metabolism has recently broadened interests beyond glucose and the Warburg effect to other nutrients, including glutamine. Because oncogenic alterations of metabolism render cancer cells addicted to nutrients, pathways involved in glycolysis or glutaminolysis could be exploited for therapeutic purposes. In this Review, we provide an updated overview of glutamine metabolism and its involvement in tumorigenesis in vitro and in vivo, and explore the recent potential applications of basic science discoveries in the clinical setting.
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Glutamine metabolism is upregulated by various oncogenic signaling pathways.
“Glutamine metabolism is upregulated by various oncogenic signaling pathways (Altman et al., 2016).”
From Targeting Metabolism for Cancer Therapy (2017) · cites this paper as Altman et al., 2016
Providing alpha-ketoglutarate, oxaloacetate, or pyruvate rescues cancer cell proliferation under glutamine starvation, confirming that glutamine supports proliferation by replenishing depleted TCA cycle intermediates (anaplerosis).
“Providing cells with αKG, oxaloacetate, or pyruvate is sufficient to rescue cancer cell proliferation in conditions of glutamine starvation, confirming that glutamine supports proliferation by replenishing depleted TCA cycle intermediates, a process termed anaplerosis (Altman et al., 2016; Weinberg et al., 2010; Yuneva et al., 2007).”
From Targeting Metabolism for Cancer Therapy (2017) · cites this paper as Altman et al., 2016
Glutamine carbon contributes to aspartate, glutamate, and tricarboxylic acid cycle metabolites via glutaminolysis.
“Glutamine carbon has been found to contribute to aspartate, glutamate and tricarboxylic acid (TCA) cycle metabolites via glutaminolysis (Figure 5) (Altman et al., 2016).”
From Targeting Metabolism for Cancer Therapy (2017) · cites this paper as Altman et al., 2016
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References 259 · Cited by 2,119
Research works printed but not linked: 1
- [144]Wang R Myc controls metabolic reprogramming upon T lymphocyte activation Immunity 35 871 882 2011 22195744 PMC3248798
- Authors
- Altman, B. J., Stine, Z. E., & Dang, C. V.
- Affiliations
- Abramson Cancer Center (US)
- Corresponding author
- Dang, Chi V.
- Venue
- Nature Reviews Cancer
- Published
- 2016-07-29
- Volume
- 16
- Issue
- 10
- Pages
- 619-634
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- PMC
- PMC5484415
- OpenAlex
- W2503851771
- Cited by
- 2,119
- References
- 259
- Citations by year
- 2026: 137 · 2025: 226 · 2024: 240 · 2023: 262 · 2022: 292 · 2021: 274 · 2020: 233 · 2019: 179 · 2018: 134 · 2017: 128 · 2016: 12 · 2014: 1
- FWCI
- 13.86
- Type
- journal article
- Language
- en
- Update notices
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R01CA057341, F32CA174148, F32CA180370, R01CA051497)
- 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 › Cancer Research and Treatments
- Keywords
- glutamine metabolism, glutaminolysis, cancer metabolism, carcinogenesis, cancer therapy, metabolic reprogramming, Warburg effect, glycolysis, clinical translation
- MeSH terms
- Adenosine Triphosphate, Citric Acid Cycle, Glutamine, Glutarates, Humans, Neoplasms
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