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. 2021 Aug 20;12:699746. doi: 10.3389/fimmu.2021.699746

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Copyright © 2021 Razeghian, Suksatan, Sulaiman Rahman, Bokov, Abdelbasset, Hassanzadeh, Marofi, Yazdanifar and Jarahian

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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The mechanism of TRAIL-induced apoptosis in tumor cells. TRAIL connecting to DR4 and DR5 stimulates apoptosis in both the extrinsic and intrinsic pathways following trimerization of receptors and FADD translocation and activation. However, various anti-apoptotic proteins, including c-FLIP, XIAP, Mcl-1, survivin, Bcl-2, and Bcl-xL can negatively regulate apoptosis pathways. TRAIL, Tumor necrosis factor-related apoptosis-inducing ligand; DRs, Death receptors; FADD, FAS-associating death domain-containing protein; c-FLIP, Cellular FLICE (FADD-like IL-1b-converting enzyme)-inhibitory protein; Bcl-2, B-cell lymphoma-2; Bcl-xl, B-cell lymphoma-extra large; Mcl-1, Myeloid-cell leukemia 1; XIAP, X-linked inhibitor of apoptosis; Bax, Bcl-2 associated X; Bak, Bcl-2 homologous antagonist/killer; Bid, BH3-interacting domain death agonist.