Why do cancers have high aerobic glycolysis? - PubMed (original) (raw)
Review
doi: 10.1038/nrc1478.
Affiliations
- PMID: 15516961
- DOI: 10.1038/nrc1478
Review
Why do cancers have high aerobic glycolysis?
Robert A Gatenby et al. Nat Rev Cancer. 2004 Nov.
Abstract
If carcinogenesis occurs by somatic evolution, then common components of the cancer phenotype result from active selection and must, therefore, confer a significant growth advantage. A near-universal property of primary and metastatic cancers is upregulation of glycolysis, resulting in increased glucose consumption, which can be observed with clinical tumour imaging. We propose that persistent metabolism of glucose to lactate even in aerobic conditions is an adaptation to intermittent hypoxia in pre-malignant lesions. However, upregulation of glycolysis leads to microenvironmental acidosis requiring evolution to phenotypes resistant to acid-induced cell toxicity. Subsequent cell populations with upregulated glycolysis and acid resistance have a powerful growth advantage, which promotes unconstrained proliferation and invasion.
Similar articles
- Metabolic changes during carcinogenesis: potential impact on invasiveness.
Smallbone K, Gatenby RA, Gillies RJ, Maini PK, Gavaghan DJ. Smallbone K, et al. J Theor Biol. 2007 Feb 21;244(4):703-13. doi: 10.1016/j.jtbi.2006.09.010. Epub 2006 Sep 16. J Theor Biol. 2007. PMID: 17055536 - The glycolytic phenotype in carcinogenesis and tumor invasion: insights through mathematical models.
Gatenby RA, Gawlinski ET. Gatenby RA, et al. Cancer Res. 2003 Jul 15;63(14):3847-54. Cancer Res. 2003. PMID: 12873971 - Hypoxia and adaptive landscapes in the evolution of carcinogenesis.
Gillies RJ, Gatenby RA. Gillies RJ, et al. Cancer Metastasis Rev. 2007 Jun;26(2):311-7. doi: 10.1007/s10555-007-9065-z. Cancer Metastasis Rev. 2007. PMID: 17404691 Review. - Metabolism and its sequelae in cancer evolution and therapy.
Gillies RJ, Gatenby RA. Gillies RJ, et al. Cancer J. 2015 Mar-Apr;21(2):88-96. doi: 10.1097/PPO.0000000000000102. Cancer J. 2015. PMID: 25815848 Free PMC article. Review.
Cited by
- How Does Cancer Occur? How Should It Be Treated? Treatment from the Perspective of Alkalization Therapy Based on Science-Based Medicine.
Hamaguchi R, Isowa M, Narui R, Morikawa H, Okamoto T, Wada H. Hamaguchi R, et al. Biomedicines. 2024 Sep 26;12(10):2197. doi: 10.3390/biomedicines12102197. Biomedicines. 2024. PMID: 39457509 Free PMC article. Review. - RNA sequencing reveals transcriptomic changes in PC-12 cells following plasminogen activator, tissue type overexpression.
Mao Y, Fang C, Zhao J, Huang X, He W, Wang C, Sun F, Dai J. Mao Y, et al. Transl Cancer Res. 2024 Sep 30;13(9):4866-4877. doi: 10.21037/tcr-24-326. Epub 2024 Sep 21. Transl Cancer Res. 2024. PMID: 39430838 Free PMC article. - Direct visualization of emergent metastatic features within an ex vivo model of the tumor microenvironment.
Anandi L, Garcia J, Ros M, Janská L, Liu J, Carmona-Fontaine C. Anandi L, et al. Life Sci Alliance. 2024 Oct 17;8(1):e202403053. doi: 10.26508/lsa.202403053. Print 2025 Jan. Life Sci Alliance. 2024. PMID: 39419548 Free PMC article. - The Interlinking Metabolic Association between Type 2 Diabetes Mellitus and Cancer: Molecular Mechanisms and Therapeutic Insights.
Asiri A, Al Qarni A, Bakillah A. Asiri A, et al. Diagnostics (Basel). 2024 Sep 25;14(19):2132. doi: 10.3390/diagnostics14192132. Diagnostics (Basel). 2024. PMID: 39410536 Free PMC article. Review. - The Use of Patient-Derived Organoids in the Study of Molecular Metabolic Adaptation in Breast Cancer.
Glibetic N, Bowman S, Skaggs T, Weichhaus M. Glibetic N, et al. Int J Mol Sci. 2024 Sep 29;25(19):10503. doi: 10.3390/ijms251910503. Int J Mol Sci. 2024. PMID: 39408832 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Molecular Biology Databases