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Nat Rev Clin Oncol. 2017 Jan;14(1):11-31. doi: 10.1038/nrclinonc.2016.60. Epub 2016 May 4.

Cancer metabolism: a therapeutic perspective.

Author information

1
The Sidney Kimmel Cancer Center, Thomas Jefferson University, 233 South 10th Street, Philadelphia, Pennsylvania 19107, USA.
2
The Breast Cancer Now Manchester Research Unit, Institute of Cancer Sciences, Cancer Research UK Manchester Institute, University of Manchester, Paterson Building, Wilmslow Road, Manchester M20 4BX, UK.
3
The Manchester Centre for Cellular Metabolism (MCCM), Institute of Cancer Sciences, Cancer Research UK Manchester Institute, University of Manchester, Paterson Building, Wilmslow Road, Manchester M20 4BX, UK.
4
School of Environment and Life Sciences, University of Salford, Cockcroft Building, Salford M5 4WT, UK.

Erratum in

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.

PMID:
27141887
DOI:
10.1038/nrclinonc.2016.60
[Indexed for MEDLINE]

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