Metabolic regulation of suppressive myeloid cells in cancer. (June 2017)

• Record Type: Journal Article
• Authors: Sica, Antonio; Strauss, Laura; Consonni, Francesca Maria; Travelli, Cristina; Genazzani, Armando; Porta, Chiara
• Is Part Of: Cytokine & growth factor reviews. Volume 35(2017)
• Page Start: 27
• Page End: 35
• Publication Date: 2017-06
• Subjects: ADRP adipose differentiation related protein -- AMPK adenosine monophosphate kinase -- AP1 activator protein 1 -- Arg1 arginase 1 -- ATP adenosine triphosphate -- CARKL carbohydrate kinase-like -- Cat2 cationic amino acid transporter 2 -- C/EBP CCAAT/enhancer-binding protein -- ER endoplasmic reticulum -- FAO fatty acid-oxidation -- G-CSF granulocyte-colony stimulating factor -- G-CSFR G-CSF receptor -- GM-CSF granulocyte macrophage-colony stimulating factor -- FFA free fatty acid -- HIF-1α hypoxia inducible factor-1α -- IGFBP3 insulin-like growth factor-binding protein 3 -- iNOS inducible nitric oxide synthase -- IRF5 interferon regulatory factor 5 -- LAL lysosomal acid lipase -- M-CSF macrophage-colony stimulating factor -- MCT monocarboxylate transporters -- MDSC myeloid-derived suppressor cells -- M-MDSC monocytic-MDSC -- mTOR mammalian target of rapamicin -- NAD nicotinamide adenine dinucleotide -- GSH glutathion -- NADPH nicotinamide adenine dinucleotide phosphate -- NAMPT nicotinamide phosphoribosyltransferase -- NO nitric oxide -- OXPHOS oxidative phosphorylation -- PGC-1β peroxisome proliferator-activated receptor γ coactivators-1β -- PMN-MDSC granulocytic-MDSC -- PPARγ peroxisome proliferator-activated receptor -- SIRT sirtuins -- STAT3 signal transducer and activator of transcription 3 -- TAM tumor-associated macrophages; TAM -- MDSC -- Metabolism -- Cancer; Cytokines -- Periodicals; 571.84
• DOI: 10.1016/j.cytogfr.2017.05.002
• Languages: English
• ISSNs: 1359-6101

Abstract

Graphical abstract: Highlights: Metabolic communication between cancer and infiltrating myeloid cells contributes to cancer immune evasion. Tumor and immune cells share similar nutrients and metabolic pathways, that support their proliferation and survival. This metabolic competition within the tumor microenvironment may fine-tune the activation and anti-tumor immune responses. Metabolic drugs acting at the metabolic crossroad between cancer and immune cells might own a bivalent anticancer activity. Abstract: Cancer cells rewire their metabolism to promote growth, survival, proliferation and long-term maintenance. The common feature of this altered metabolism is the increased glucose uptake and fermentation of glucose to lactate, which is observed even in the presence of completely functioning mitochondria. This effect is known as the 'Warburg Effect' and its intensive investigation in the last decade has partially established either its causes or its functions. It is now emerging that a major side effect of the Warburg Effect is immunosuppression, which limits the immunogenicity of cancer cells and therefore restricts the therapeutic efficacy of anticancer immunotherapy. Here we discuss how the metabolic communication between cancer and infiltrating myeloid cells contributes to cancer immune evasion and how the understanding of these mechanisms may improve current immunotherapies.