PKCβII-ACSL4 pathway mediating ferroptosis execution and anti-tumor immunity

查看全文 作　　者：Guang [1]Lei;Amber [1]Horbath;Zhuang [1]Li;Boyi [1,2]Gan

机构地区：[1]Department of Experimental Radiation Oncology,The University of Texas MD Anderson Cancer Center,Houston,TX 77030,USA;[2]The University of TexasMD Anderson UTHealth Graduate School of Biomedical Sciences,Houston,TX 77030,USA

出　　处：《Cancer Communications》索引2022年第42卷第7期,共4页

基　　金：supported by The University of TexasMDAnderson Cancer Center,National Institutes of Health grants R01CA181196,R01CA244144,and R01CA247992;Cancer Prevention&Research Institute of Texas grant RP220258(to Boyi Gan);by Cancer Center Support(Core)Grant P30 CA016672 from the National Cancer Institute(to The University of Texas MD Anderson Cancer Center). 摘　　要：Ferroptosis is an iron-dependent form of regulated cell death that results from oxidative damages of membrane phospholipids,and is mechanistically and morphologically unique compared to other cell death modalities,such as apoptosis and necroptosis[1].Excessive ferroptosis is indicative of many pathological conditions,including cardiovascular diseases,neurodegenerative diseases,and acute organ injury,whereas ferroptosis impairment has been shown to fuel tumor progression and metastasis;therefore,targeting ferroptosis represents a promising strategy for treating these diseases[2-10].Ferroptosis is triggered by a lethal accumulation of lipid peroxides on the cell membrane. 关键词：IMMUNITY DISEASES DEATH

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PKCβII-ACSL4 pathway mediating ferroptosis execution and anti-tumor immunity

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