Metabolic signatures of cancer cells and stem cells
Open accessAbstract
In contrast to terminally differentiated cells, cancer cells and stem cells retain the ability to re-enter the cell cycle and proliferate. In order to proliferate, cells must increase the uptake and catabolism of nutrients to support anabolic cell growth. Intermediates of central metabolic pathways have emerged as key players that can influence cell differentiation 'decisions', processes relevant for both oncogenesis and normal development. Consequently, how cells rewire metabolic pathways to support proliferation may have profound consequences for cellular identity. Here, we discuss the metabolic programs that support proliferation and explore how metabolic states are intimately entwined with the cell fate decisions that characterize stem cells and cancer cells. By comparing the metabolism of pluripotent stem cells and cancer cells, we hope to illuminate common metabolic strategies as well as distinct metabolic features that may represent specialized adaptations to unique cellular demands.
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Being able to fine-tune the function of metabolic pathways like the TCA cycle-in particular, to toggle between catabolic and anabolic activity-set the stage for early unicellular life forms to evolve into multicellular organisms.
“Being able to fine-tune the function of metabolic pathways like the TCA cycle—in particular, to toggle between catabolic and anabolic activity—set the stage for early unicellular life forms to evolve into multicellular organisms, which require coordination of metabolic activity beyond that dictated by local nutrient availability (29, 30).”
From Regulation and function of the mammalian tricarboxylic acid cycle (2023) · cites this paper as [30]
Glutamine is the preferred anaplerotic substrate in most proliferating cells growing in culture.
“The preferred anaplerotic substrate in most proliferating cells growing in culture is glutamine, the most abundant circulating amino acid in mammals (30, 72, 73, 74).”
From Regulation and function of the mammalian tricarboxylic acid cycle (2023) · cites this paper as [30]
By blocking the enzymatic activity of histone and DNA demethylases, d-2HG can lock cells in a hypermethylated state that blocks differentiation and reinforces a malignant and stem cell-like phenotype.
“By blocking the enzymatic activity of histone and DNA demethylases, d-2HG can function to lock cells in a hypermethylated state that blocks differentiation and reinforces a malignant and stem cell–like phenotype (30, 172, 173, 174).”
From Regulation and function of the mammalian tricarboxylic acid cycle (2023) · cites this paper as [30]
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References 176 · Cited by 322
- Authors
- Intlekofer, A. M., & Finley, L. W. S.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Intlekofer, Andrew M.
- Finley, Lydia W. S.
- Venue
- Nature Metabolism
- Published
- 2019-02-11
- Volume
- 1
- Issue
- 2
- Pages
- 177-188
- ISSN
- 2522-5812 (ISSN-L)
- PMC
- PMC6594714
- OpenAlex
- W2913043277
- Cited by
- 322
- References
- 176
- Citations by year
- 2026: 27 · 2025: 29 · 2024: 59 · 2023: 53 · 2022: 47 · 2021: 52 · 2020: 43 · 2019: 11 · 2015: 1
- FWCI
- 3.63
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Foundation Medicine
- National Cancer Institute (K08CA201483, P30CA008748)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Keywords
- cancer metabolism, stem cell metabolism, pluripotent stem cells, cell proliferation, metabolic reprogramming, cell differentiation, cell fate determination, self-renewal, carcinogenesis, anabolic metabolism, central metabolic pathways
- MeSH terms
- Nutrients, Cell Cycle, Cell Differentiation, Cell Survival, Humans, Neoplasms, Stem Cells, Cell Proliferation, Metabolic Networks and Pathways
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