Heterogeneity of tumor-induced gene expression changes in the human metabolic network
Open accessAbstract
Reprogramming of cellular metabolism is an emerging hallmark of neoplastic transformation. However, it is not known how the expression of metabolic genes in tumors differs from that in normal tissues, or whether different tumor types exhibit similar metabolic changes. Here we compare expression patterns of metabolic genes across 22 diverse types of human tumors. Overall, the metabolic gene expression program in tumors is similar to that in the corresponding normal tissues. Although expression changes of some metabolic pathways (e.g., upregulation of nucleotide biosynthesis and glycolysis) are frequently observed across tumors, expression changes of other pathways (e.g., oxidative phosphorylation) are very heterogeneous. Our analysis also suggests that the expression changes of some metabolic genes (e.g., isocitrate dehydrogenase and fumarate hydratase) may enhance or mimic the effects of recurrent mutations in tumors. On the level of individual biochemical reactions, many hundreds of metabolic isoenzymes show significant and tumor-specific expression changes. These isoenzymes are potential targets for anticancer therapy.
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Metabolic gene expression signatures are more similar to the tissue of origin than to tumors from different organs.
“Gene expression signatures focused on the metabolic network also bear more similarity to the tissue of origin than to tumors from different organs (4).”
From Metabolic reprogramming and cancer progression (2020) · cites this paper as [4]
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- Authors
- Hu, J., Locasale, J. W., Bielas, J. H., O'Sullivan, J., Sheahan, K., Cantley, L. C., Heiden, M. G. V., & Vitkup, D.
- Affiliations
- Columbia University (US)
- Cornell University (US)
- University of Washington (US)
- St. Vincent's University Hospital (IE)
- Beth Israel Deaconess Medical Center (US)
- Dana-Farber Cancer Institute (US)
- Corresponding author
- Vitkup, Dennis
- ORCID
- Venue
- Nature Biotechnology
- Published
- 2013-04-21
- Volume
- 31
- Issue
- 6
- Pages
- 522-529
- ISSN
- 0733-222X (ISSN-L)
- 1087-0156
- 1546-1696
- PMC
- PMC3681899
- OpenAlex
- W2003605385
- Cited by
- 407
- References
- 51
- Citations by year
- 2026: 10 · 2025: 16 · 2024: 29 · 2023: 25 · 2022: 29 · 2021: 44 · 2020: 42 · 2019: 40 · 2018: 37 · 2017: 34 · 2016: 36 · 2015: 37 · 2014: 20 · 2013: 7
- FWCI
- 11.71
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Biotechnology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion)
- PMC
- Funders
- Burroughs Wellcome Fund
- Damon Runyon Cancer Research Foundation
- National Cancer Institute (R00CA168997, U54CA121852)
- National Institute of General Medical Sciences (GM079759, R01GM079759)
- National Institute of Environmental Health Sciences (R01ES019319)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bioinformatics and Genomic Networks
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Keywords
- cancer metabolism, metabolic gene expression, metabolic reprogramming, tumor heterogeneity, metabolic networks, glycolysis, oxidative phosphorylation, nucleotide synthesis, isocitrate dehydrogenase, fumarate hydratase, anticancer drug targets
- MeSH terms
- Cell Transformation, Neoplastic, Glycolysis, Humans, Isocitrate Dehydrogenase, Isoenzymes, Mutation, Neoplasms, Oxidative Phosphorylation, Gene Expression Regulation, Neoplastic, Computational Biology, Oligonucleotide Array Sequence Analysis, Metabolic Networks and Pathways, Molecular Targeted Therapy
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