Metabolic reprogramming in the tumour microenvironment: a hallmark shared by cancer cells and T lymphocytes

被引:88
作者
Allison, Katrina E. [1 ]
Coomber, Brenda L. [2 ]
Bridle, Byram W. [1 ]
机构
[1] Univ Guelph, Dept Pathobiol, Ontario Vet Coll, Rm 3808,Bldg 89,50 Stone Rd E, Guelph, ON N1G 2W1, Canada
[2] Univ Guelph, Dept Biomed Sci, Ontario Vet Coll, Guelph, ON, Canada
关键词
cancer; T cells; tumour immunology; ACTIVATED PROTEIN-KINASE; PROSTATE-CANCER; MITOCHONDRIAL BIOGENESIS; TRYPTOPHAN CATABOLISM; AEROBIC GLYCOLYSIS; EFFECTOR FUNCTION; METFORMIN; MELANOMA; GROWTH; AMPK;
D O I
10.1111/imm.12777
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Altered metabolism is a hallmark of cancers, including shifting oxidative phosphorylation to glycolysis and up-regulating glutaminolysis to divert carbon sources into biosynthetic pathways that promote proliferation and survival. Therefore, metabolic inhibitors represent promising anti-cancer drugs. However, T cells must rapidly divide and survive in harsh microenvironments to mediate anti-cancer effects. Metabolic profiles of cancer cells and activated T lymphocytes are similar, raising the risk of metabolic inhibitors impairing the immune system. Immune checkpoint blockade provides an example of how metabolism can be differentially impacted to impair cancer cells but support T cells. Implications for research with metabolic inhibitors are discussed.
引用
收藏
页码:175 / 184
页数:10
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