Metabolic flux and the regulation of mammalian cell growth
Open accessAbstract
The study of normal mammalian cell growth and the defects that contribute to disease pathogenesis links metabolism to cell growth. Here, we visit several aspects of growth-promoting metabolism, emphasizing recent advances in our understanding of how alterations in glucose metabolism affect cytosolic and mitochondrial redox potential and ATP generation. These alterations drive cell proliferation not only through supporting biosynthesis, energy metabolism, and maintaining redox potential but also through initiating signaling mechanisms that are still poorly characterized. The evolutionary basis of these additional layers of growth control is also discussed.
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Aerobic glycolysis is a prominent feature of cancer cell metabolism, and its main role is thought to be support of biosynthetic pathways required for cellular proliferation.
“AG is a prominent feature of cancer cell metabolism; its main role is thought to be support of biosynthetic pathways required for cellular proliferation”
From Aerobic glycolysis in the human brain is associated with development and neotenous gene expression (2014) · cites this paper as Locasale and Cantley, 2011
The Warburg Effect and cell growth section describes aerobic glycolysis as a common feature of tumor cells and identifies support of biosynthesis as one of its functions. It also says those functions are multiple and debated, including redox balance, energy balance, and signaling; it does not identify biosynthesis as the main role. No page number is available in our copy. (LLM, conf=0.88)
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- Authors
- Locasale, J. W., & Cantley, L. C.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- Corresponding author
- Locasale, Jason W.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2011-10
- Volume
- 14
- Issue
- 4
- Pages
- 443-451
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC3196640
- OpenAlex
- W2028974980
- Cited by
- 449
- References
- 11
- Citations by year
- 2026: 16 · 2025: 33 · 2024: 21 · 2023: 35 · 2022: 32 · 2021: 39 · 2020: 38 · 2019: 28 · 2018: 38 · 2017: 31 · 2016: 32 · 2015: 26 · 2014: 24 · 2013: 33 · 2012: 22
- FWCI
- 1.90
- 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, 655 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)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute
- National Institutes of Health
- American Cancer Society
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- metabolic flux, mammalian cell growth, glucose metabolism, mitochondrial redox potential, ATP production, cell proliferation, biosynthesis, energy metabolism, metabolic signaling
- MeSH terms
- Adenosine Triphosphate, Animals, Energy Metabolism, Glucose, Humans, Signal Transduction, Cell Proliferation, Membrane Potential, Mitochondrial
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