Cancer metabolism: a therapeutic perspective

By U. Martinez-Outschoorn, Maria Peiris‐Pagès, R. Pestell, F. Sotgia, M. Lisanti. Nature Reviews Clinical Oncology, 2017

1,404 citations recorded by the source corpus.

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.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/6c40a699771b4c44456790e509345944707a2fe8

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Citations in the corpus

Oxidative Phosphorylation as an Emerging Target in Cancer Therapy (2018, background): “Lonidamine is classically described as an inhibitor of glycolytic hexokinases but has recently been shown to inhibit complex II in isolated mitochondria and in DB-1 melanoma cells (5, 61).”
ESPEN expert group recommendations for action against cancer-related malnutrition. (2017, background): “The use of standard formulas for the calculation of energy needs may be inaccurate given the altered energy metabolism and metabolic differences in patients with different cancer types [35,58,59].”
T Cell Dysfunction in Cancer (2018, background): “This creates an environment with low glucose, low amino acids, low oxygen, and low pH, which are all considered metabolic checkpoints (Kato et al., 2013; Martinez-Outschoorn et al., 2017; Scharping and Delgoffe, 2016; Wilson and Hay, 2011).”
Packaging and transfer of mitochondrial DNA via exosomes regulate escape from dormancy in hormonal therapy-resistant breast cancer (2017, neutral): “S2 A and B ) (14, 15).”
Mitochondrial metabolism and cancer (2017, background): “The reversibility of many reactions of the tricarboxylic acid (TCA) cycle and the existence of multiple anaplerotic circuitries centered on mitochondria ensure such a metabolic adaptation [25, 81].”
Mitochondrial stress induced by continuous stimulation under hypoxia rapidly drives T cell exhaustion (2021, neutral): “In cancer, elevated tumor cell metabolism can dramatically alter the nutrient milieu T cells experience 14 .”
Targeting Metabolism for Cancer Therapy (2017, background): “Some recent examples to illustrate how these differences might be exploited for therapy are highlighted, but many other targets have been proposed and are discussed in detail elsewhere (Bobrovnikova-Marjon and Hurov, 2014; Galluzzi et al., 2013; Martinez-Outschoorn et al., 2017).”