Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017 Jan;14(1):11-31.
doi: 10.1038/nrclinonc.2016.60. Epub 2016 May 4.

Cancer metabolism: a therapeutic perspective

Ubaldo E Martinez-Outschoorn  1 , Maria Peiris-Pagés  2   3 , Richard G Pestell  1 , Federica Sotgia  2   3   4 , Michael P Lisanti  2   3
Affiliations
Review

Cancer metabolism: a therapeutic perspective

Ubaldo E Martinez-Outschoorn et al. Nat Rev Clin Oncol. 2017 Jan.

Erratum in

  • Cancer metabolism: a therapeutic perspective.
    Martinez-Outschoorn UE, Peiris-Pagés M, Pestell RG, Sotgia F, Lisanti MP. Martinez-Outschoorn UE, et al. Nat Rev Clin Oncol. 2017 Feb;14(2):113. doi: 10.1038/nrclinonc.2017.1. Epub 2017 Jan 17. Nat Rev Clin Oncol. 2017. PMID: 28094266 No abstract available.

Abstract

Awareness that the metabolic phenotype of cells within tumours is heterogeneous - and distinct from that of their normal counterparts - is growing. In general, tumour cells metabolize glucose, lactate, pyruvate, hydroxybutyrate, acetate, glutamine, and fatty acids at much higher rates than their nontumour equivalents; however, the metabolic ecology of tumours is complex because they contain multiple metabolic compartments, which are linked by the transfer of these catabolites. This metabolic variability and flexibility enables tumour cells to generate ATP as an energy source, while maintaining the reduction-oxidation (redox) balance and committing resources to biosynthesis - processes that are essential for cell survival, growth, and proliferation. Importantly, experimental evidence indicates that metabolic coupling between cell populations with different, complementary metabolic profiles can induce cancer progression. Thus, targeting the metabolic differences between tumour and normal cells holds promise as a novel anticancer strategy. In this Review, we discuss how cancer cells reprogramme their metabolism and that of other cells within the tumour microenvironment in order to survive and propagate, thus driving disease progression; in particular, we highlight potential metabolic vulnerabilities that might be targeted therapeutically.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Nature. 2009 Oct 29;461(7268):1282-6 - PubMed
    1. Science. 2014 Mar 28;343(6178):1485-9 - PubMed
    1. Trends Pharmacol Sci. 2015 Feb;36(2):124-35 - PubMed
    1. Cell Metab. 2014 Dec 2;20(6):953-66 - PubMed
    1. Cancer Cell. 2015 Jan 12;27(1):57-71 - PubMed

MeSH terms

-