Cancer metabolism: a therapeutic perspective

Martinez-Outschoorn, Ubaldo E.; Peiris-Pagés, Maria; Pestell, Richard G.; Sotgia, Federica; Lisanti, Michael P.

doi:10.1038/nrclinonc.2016.60

Cited by 1,505Cancer, Hypoxia, and MetabolismMetabolism, Diabetes, and CancerCancer, Lipids, and Metabolism

Cancer metabolism: a therapeutic perspective

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Martinez-Outschoorn, Ubaldo E., Peiris-Pagés, Maria, Pestell, Richard G., Sotgia, Federica, Lisanti, Michael P.·2017·Nature Reviews Clinical Oncology

DOI 10.1038/nrclinonc.2016.60

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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.

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Malignant cells share a common metabolic trait, namely that they can acquire and use nutrients from a predominantly nutrient-poor environment.
“Notwithstanding the diversity of cancers, malignant cells share a common metabolic trait, namely that they can acquire and use nutrients from a predominantly nutrient-poor environment, a modus operandi that emerged as a promising target to battle tumors (202–205).”
From Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease (2018) · cites this paper as [204]

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Authors: Martinez-Outschoorn, U. E., Peiris-Pagés, M., Pestell, R. G., Sotgia, F., & Lisanti, M. P.
Affiliations: Thomas Jefferson University (US)
University of Manchester (GB)
Corresponding author: Sotgia, Federica
Lisanti, Michael P.
ORCID: Pestell, Richard G.
Sotgia, Federica
Lisanti, Michael P.
Venue: Nature Reviews Clinical Oncology
Publisher: Springer Science and Business Media LLC
Published: 2016-05-04
Volume: 14
Issue: 1
Pages: 11-31
ISSN: 1759-4774 (ISSN-L)
1759-4782
DOI: 10.1038/nrclinonc.2016.60
OpenAlex: W2345381093
Cited by: 1,505
References: 228
Citations by year: 2026: 95 · 2025: 137 · 2024: 153 · 2023: 162 · 2022: 170 · 2021: 180 · 2020: 190 · 2019: 155 · 2018: 134 · 2017: 107 · 2016: 19
FWCI: 12.70
Type: journal article
Language: en
Update notices: erratum (2017-01-17)
Open access: green
usir.salford.ac.uk
Licence: cc-by
www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Nature Reviews Clinical Oncology (publishedVersion)
PubMed (publishedVersion)
Research Explorer (The University of Manchester) (publishedVersion)
University of Salford Institutional Repository (University of Salford) (submittedVersion, cc-by)
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 › Cancer Research › Cancer, Lipids, and Metabolism
Keywords: cancer metabolism, metabolic reprogramming, tumor microenvironment, metabolic heterogeneity, glucose metabolism, glutamine metabolism, fatty acid metabolism, redox homeostasis, metabolic coupling, metabolic vulnerability, anticancer drug targets, tumor progression
MeSH terms: Mitochondrial Ribosomes, Acetyl Coenzyme A, Adaptation, Physiological, Amino Acids, Antineoplastic Agents, Antioxidants, Autophagy, Blood Glucose, Energy Metabolism, Fatty Acids, Glutamine, Humans, Ketone Bodies, Lipids, Mitochondria, Neoplasms, Nucleic Acids, Transcription Factors, Oxidative Stress, Glutamic Acid, Genetic Heterogeneity, Pyruvic Acid, Lactic Acid, Epigenomics, TOR Serine-Threonine Kinases, Tumor Microenvironment

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