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The biology of cancer: metabolic reprogramming fuels cell growth and proliferation.

Author information

Affiliations

  • 1. Department of Cancer Biology, Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA 19104-6160, USA.
      Authors
    • DeBerardinis RJ 1
    (1 author)

ORCIDs linked to this article

Cell Metabolism, 01 Jan 2008, 7(1):11-20
https://doi.org/10.1016/j.cmet.2007.10.002 PMID: 18177721 

Review

Abstract 

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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Read article at publisher's site: https://doi.org/10.1016/j.cmet.2007.10.002

Read article for free, from open access legal sources, via Unpaywall: http://www.cell.com/article/S1550413107002951/pdfUnpaywall

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    Funding 

    Funders who supported this work.

    Damon Runyon Cancer Research Foundation

      NCI NIH HHS (1)

      NIDDK NIH HHS (1)

      National Institutes of Health (2)