ACSL4,PUFA,and ferroptosis:new arsenal in anti-tumor immunity  

作　　者：Boyi Gan 

机构地区：[1]Department of Experimental Radiation Oncology,The University of Texas MD Anderson Cancer Center,Houston,TX,USA

出　　处：《Signal Transduction and Targeted Therapy》2022年第5期1363-1365,共3页信号转导与靶向治疗（英文）

基　　金：The author thanks Guang Lei for generating the figure used in this paper and apologizes to colleagues whose work cannot be cited in this manuscript due to space limitations.Research in the author’s lab has been supported by The University of Texas MD Anderson Cancer Center,National Institutes of Health grants R01CA181196,R01CA244144,and R01CA247992;Cancer Prevention&Research Institute of Texas grant RP220258(to B.G.);by Cancer Center Support(Core)Grant P30 CA016672 from the National Cancer Institute(to The University of Texas MD Anderson Cancer Center).

摘　　要：In a recent study published in Cancer Cell,Liao et al.1 identified CD8+T-cell-derived interferon(IFN)γin combination with polyunsaturated fatty acids(PUFAs)as a natural ferroptosis inducer(FIN)to trigger tumor ferroptosis and promote anti-tumor immunity in an acyl-coenzyme A synthetase long-chain family member 4(ACSL4)-dependent manner.Ferroptosis refers to a form of regulated cell death triggered by excessive iron-dependent peroxidation of PUFA-containing phospholipids(PUFA-PLs)in the cellular membrane.

关 键 词：IMMUNITY PEROXIDATION 

分 类 号：R730.51[医药卫生—肿瘤]