Cancer cell metabolic reprogramming: a keystone for the response to immunotherapy

被引:77
作者
Cerezo, Michael [1 ,2 ]
Rocchi, Stephane [2 ]
机构
[1] INSERM, U981, Villejuif, France
[2] Univ Cote dAzur, INSERM, U1065, Ctr Mediterraneen Med Mol,Team 12, Nice, France
关键词
TUMORAL IMMUNE RESISTANCE; ARYL-HYDROCARBON RECEPTOR; CD8(+) T-CELLS; INDOLEAMINE 2,3-DIOXYGENASE; L-ARGININE; LACTIC-ACID; TRYPTOPHAN DEGRADATION; ANTITUMOR IMMUNITY; SUPPRESSOR-CELLS; MYELOID CELLS;
D O I
10.1038/s41419-020-03175-5
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
By targeting the tumor microenvironment to stimulate antitumor immunity, immunotherapies have revolutionized cancer treatment. However, many patients do not respond initially or develop secondary resistance. Based on the limited resources in the tumor microenvironment and competition between tumor and immune cells, the field of immune metabolism has produced extensive knowledge showing that targeting metabolism could help to modulate antitumor immunity. However, among all the different potentially targetable metabolic pathways, it remains unclear which have more potential to overcome resistance to immune checkpoint inhibitors. Here, we explore metabolic reprogramming in cancer cells, which might inhibit antitumor immunity, and strategies that can be used to favor the antitumor response.
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页数:10
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