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. 2021 Nov 2;9:739392. doi: 10.3389/fcell.2021.739392

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Copyright © 2021 Liu, Duan, Dai and Zeng.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Crosstalk between ferroptosis and tumor immunity. Ferroptotic cancer cells release the KRAS-G12D proteins. Extracellular KRAS-G12D proteins are packaged into exosomes, which are absorbed by macrophages through an AGER-dependent mechanism, thereby inducing macrophages to switch to the M2 phenotype to accelerate cancer development. Ferroptotic cancer cells can also release HMGB1 and 8-OHG to affect the innate immune cells’ functions in the TME. In addition, ferroptotic cancer cells released PGE2 can inhibit the infiltration of cDC1s by suppressing the chemokines CCL5 and XCL1 that secreted by NK cells. PGE2 can also downregulate chemokine receptors to block cDC1s directly. Many cell types (such as macrophages) release TGF-β1 to activate SMAD proteins to inhibit the expression of SLC7A11, thereby promoting the ferroptosis of cancer cells. AGER, advanced glycosylation end-product-specific receptor; HMGB1, high mobility group box1; 8-OHG, 8-Hydroxyguanosine; cDC1s, conventional type 1 dendritic cells; PGE2, Prostaglandin E2; TGF-β1, transforming growth factor-β1.