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The Biology of Cancer: Metabolic Reprogramming Fuels Cell Growth and Proliferation
Open accessAbstract
Cell proliferation requires nutrients, energy, and biosynthetic activity to duplicate all macromolecular components during each passage through the cell cycle. It is therefore not surprising that metabolic activities in proliferating cells are fundamentally different from those in nonproliferating cells. This review examines the idea that several core fluxes, including aerobic glycolysis, de novo lipid biosynthesis, and glutamine-dependent anaplerosis, form a stereotyped platform supporting proliferation of diverse cell types. We also consider regulation of these fluxes by cellular mediators of signal transduction and gene expression, including the phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR system, hypoxia-inducible factor 1 (HIF-1), and Myc, during physiologic cell proliferation and tumorigenesis.
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In the citing paper
“While the effect of the PI3K/Akt signalling pathway on glycolysis has been shown to be mediated in part via its regulation of HIF-1α expression and transcriptional activity in hypoxia [133,134], several lines of evidence have shown that its effects on glucose metabolism are also mediated via HIF-independent mechanisms.”
From HIF-1-Independent Mechanisms Regulating Metabolic Adaptation in Hypoxic Cancer Cells (2021) · cites this paper as [136]
In the citing paper
“Furthermore, studies on proliferating primary lymphocytes have shown that glucose is primarily converted to lactate, demonstrating that aerobic glycolysis is not only restricted to cancer cells (DeBerardinis et al., 2008).”
From Therapeutic targeting of hypoxia and hypoxia-inducible factors in cancer (2016) · cites this paper as DeBerardinis et al., 2008
In the citing paper
“Cancer cells preferentially metabolize glucose by aerobic glycolysis, a phenomenon known as the Warburg effect.”
From An LXR Agonist Promotes Glioblastoma Cell Death through Inhibition of an EGFR/AKT/SREBP-1/LDLR–Dependent Pathway (2011) · cites this paper as [16]
In the citing paper
“mTORC1 appears to be critical for linking PI3K signaling with tumor metabolism (16, 59, 60).”
From An LXR Agonist Promotes Glioblastoma Cell Death through Inhibition of an EGFR/AKT/SREBP-1/LDLR–Dependent Pathway (2011) · cites this paper as [16]
In the citing paper
“Regarding intrinsic metabolism, several studies have demonstrated that tumor cells drive aerobic glycolysis and promote cell proliferation via fueling mitochondrial metabolism [220, 221].”
From Tumor microenvironment signaling and therapeutics in cancer progression (2023) · cites this paper as [221]
In the citing paper
“While glutamine can be synthesized directly by most mammalian cells, it has been recognized for several decades that glutamine supplementation is necessary for the growth and viability of many cultured cell lines, particularly cancer cell lines (72, 75, 76).”
From Regulation and function of the mammalian tricarboxylic acid cycle (2023) · cites this paper as [72]
In the citing paper
“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 [72]
In the citing paper
“The flow of glucose to the cytosolic acetyl-CoA pool is regulated by using TCA cycle intermediates and a truncated TCA cycle (46).”
From Fueling Immunity: Insights into Metabolism and Lymphocyte Function (2013) · cites this paper as [46]
In the citing paper
“Despite the availability of extracellular lipids for membrane biosynthesis, FFAs are generated de novo from glucose in proliferating cells using this pathway (46).”
From Fueling Immunity: Insights into Metabolism and Lymphocyte Function (2013) · cites this paper as [46]
In the citing paper
“As mentioned previously, it is now appreciated that in proliferating cells the TCA cycle functions as a source of biosynthetic precursors in addition to its role in ATP production (46).”
From Fueling Immunity: Insights into Metabolism and Lymphocyte Function (2013) · cites this paper as [46]
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“…complex; mTOR, mammalian target of rapamycin; glc-6-P, glucose-6-phosphate; 3-PG, 3-phosphoglycerate; PDK1, pyruvate dehydrogenase kinase 1; SDH, succinate dehydrogenase; FH, fumarate hydratase; HIF-1 a , hypoxia-inducible factor 1 a ; VHL, von Hippel-Lindau. et al., 2007; Selak et al., 2005).”
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Metadata
- Authors
- DeBerardinis, R. J., Lum, J. J., Hatzivassiliou, G., & Thompson, C. B.
- Affiliations
- Children's Hospital of Philadelphia (US)
- Abramson Cancer Center (US)
- Corresponding author
- Thompson, Craig B.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2008-01
- Volume
- 7
- Issue
- 1
- Pages
- 11-20
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W2014058353
- Semantic Scholar
- 2c13b73ce6123966a9f8c82b8f26d9e3fbc312b7
- Cited by
- 4,088
- References
- 85
- Citations by year
- 2026: 124 · 2025: 170 · 2024: 227 · 2023: 234 · 2022: 292 · 2021: 314 · 2020: 320 · 2019: 286 · 2018: 240 · 2017: 280 · 2016: 244 · 2015: 260 · 2014: 269 · 2013: 201 · 2012: 187
- FWCI
- 10.42
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 2024 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (K08 DK072565, PO1 CA104838)
- Damon Runyon Cancer Research Foundation
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- cancer metabolism, metabolic reprogramming, cell proliferation, aerobic glycolysis, PI3K/AKT/mTOR pathway, HIF-1, c-Myc, carcinogenesis, signal transduction
- MeSH terms
- Animals, Humans, Models, Biological, Neoplasms, Signal Transduction, Phosphatidylinositol 3-Kinases, Cell Proliferation, Hypoxia-Inducible Factor 1
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