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The Metabolic Profile of Tumors Depends on Both the Responsible Genetic Lesion and Tissue Type
Open accessAbstract
The altered metabolism of tumors has been considered a target for anticancer therapy. However, the relationship between distinct tumor-initiating lesions and anomalies of tumor metabolism in vivo has not been addressed. We report that MYC-induced mouse liver tumors significantly increase both glucose and glutamine catabolism, whereas MET-induced liver tumors use glucose to produce glutamine. Increased glutamine catabolism in MYC-induced liver tumors is associated with decreased levels of glutamine synthetase (Glul) and the switch from Gls2 to Gls1 glutaminase. In contrast to liver tumors, MYC-induced lung tumors display increased expression of both Glul and Gls1 and accumulate glutamine. We also show that inhibition of Gls1 kills cells that overexpress MYC and catabolize glutamine. Our results suggest that the metabolic profiles of tumors are likely to depend on both the genotype and tissue of origin and have implications regarding the design of therapies targeting tumor metabolism.
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In the citing paper
“Importantly, inhibiting glutamine entry into the TCA cycle can blunt tumor progression in a MYC-driven cancer model of liver cancer (Xiang et al., 2015; Yuneva et al., 2012) and a MYC-inducible Burkitt lymphoma model (Le et al., 2012; Xiang et al., 2015).”
From Targeting Metabolism for Cancer Therapy (2017) · cites this paper as Yuneva et al., 2012
In the citing paper
“MYC has been found to increase mRNA and protein levels of glutamine transporters as well as expression of the enzyme glutaminase, which catalyzes the first step in glutaminolysis (Gao et al., 2009; Wise et al., 2008; Yuneva et al., 2012).”
From Targeting Metabolism for Cancer Therapy (2017) · cites this paper as Yuneva et al., 2012
In the citing paper
“Second, although different oncogenes reprogram metabolism in different ways, the tissue in which the oncogene is expressed affects the execution of metabolic reprogramming.”
From Metabolic reprogramming and cancer progression (2020) · cites this paper as [5]
In the citing paper
“Transgenic MYC induces metabolic changes in both liver tumors and lung tumors but activates glutamine catabolism in lung tumors and glutamine synthesis in liver tumors.”
From Metabolic reprogramming and cancer progression (2020) · cites this paper as [5]
In the citing paper
“MYC-driven cancer cells exhibit enhanced glutamine utilization accompanied by increased expression of key glutaminolysis enzymes, including GLS1/GLS2 and GLUD1178–180.”
From Glutamine reliance in cell metabolism (2020) · cites this paper as [179]
In the citing paper
“For example, liver tumors with aberrant overexpression of MYC display enhanced glutamine oxidation and sensitivity to therapies that target glutamine catabolism relative to liver tumors driven by overexpression of MET (196).”
From Regulation and function of the mammalian tricarboxylic acid cycle (2023) · cites this paper as [196]
In the citing paper
“furthermore, a similar accumulation of glucose-derived glutamine within the tumor tissue was observed in a mouse model of c-Met-driven liver cancer (Yuneva et al., 2012).”
From The emerging hallmarks of cancer metabolism (2016) · cites this paper as Yuneva et al., 2012
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Metadata
- Authors
- Yuneva, M. O., Fan, T. W. M., Allen, T. D., Higashi, R. M., Ferraris, D. V., Tsukamoto, T., Matés, J. M., Alonso, F. J., Wang, C., Seo, Y., Chen, X., & Bishop, J. M.
- Affiliations
- University of California, San Francisco (US)
- University of Louisville (US)
- Johns Hopkins University (US)
- Universidad de Málaga (ES)
- Corresponding author
- Yuneva, Mariia O.
- ORCID
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2012-02
- Volume
- 15
- Issue
- 2
- Pages
- 157-170
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC3282107
- OpenAlex
- W2036659083
- Cited by
- 639
- References
- 64
- Citations by year
- 2026: 17 · 2025: 37 · 2024: 35 · 2023: 41 · 2022: 53 · 2021: 66 · 2020: 43 · 2019: 59 · 2018: 45 · 2017: 63 · 2016: 47 · 2015: 39 · 2014: 42 · 2013: 34 · 2012: 16
- FWCI
- 13.97
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R35CA044338, R01CA118434)
- National Institute of Neurological Disorders and Stroke (R21NS074151)
- National Center for Research Resources (P20RR018733)
- 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 › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- cancer metabolism, c-Myc, MET, glutamine catabolism, glutamine synthetase, glutaminase, GLS1, GLS2, liver tumors, lung cancer, genetic lesions, glutamine accumulation
- MeSH terms
- Animals, Cell Transformation, Neoplastic, Citric Acid Cycle, Glucokinase, Glucose, Glutamine, Humans, Immunohistochemistry, Isotope Labeling, Liver Neoplasms, Experimental, Lung Neoplasms, Immunoblotting, Blotting, Western, Proto-Oncogene Proteins c-myc, DNA Primers, Lactic Acid, Proto-Oncogene Proteins c-met, Nuclear Magnetic Resonance, Biomolecular, RNA Interference, Cell Line, Tumor, Mice, Metabolome
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