Ferroptosis-inducing agents enhance TRAIL-induced apoptosis through upregulation of death receptor 5

Journal of Cellular Biochemistry
Young-Sun LeeYong J Lee

Abstract

Ferroptosis is considered genetically and biochemically distinct from other forms of cell death. In this study, we examined whether ferroptosis shares cell death pathways with other types of cell death. When human colon cancer HCT116, CX-1, and LS174T cells were treated with ferroptotic agents such as sorafenib (SRF), erastin, and artesunate, data from immunoblot assay showed that ferroptotic agents induced endoplasmic reticulum (ER) stress and the ER stress response-mediated expression of death receptor 5 (DR5), but not death receptor 4. An increase in the level of DR5, which is activated by binding to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and initiates apoptosis, was probably responsible for synergistic apoptosis when cells were treated with ferroptotic agent in combination with TRAIL. This collateral effect was suppressed in C/EBP (CCAAT-enhancer-binding protein)-homologous protein (CHOP)-deficient mouse embryonic fibroblasts or DR5 knockdown HCT116 cells, but not in p53-deficient HCT116 cells. The results from in vitro studies suggest the involvement of the p53-independent CHOP/DR5 axis in the synergistic apoptosis during the combinatorial treatment of ferroptotic agent and TRAIL. The synergistic a...Continue Reading

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Citations

Jun 25, 2019·Journal of Cellular and Molecular Medicine·Tao XuJianxun Wang
Jan 12, 2019·Archives of Pharmacal Research·Kyoung-Jin MinTaeg Kyu Kwon
Jun 14, 2019·Frontiers in Neuroscience·Xiao-Yuan MaoWei-Lin Jin
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Mar 19, 2021·Cell Death & Disease·Shu XuShenghong Zhang
Dec 12, 2019·Biochemical and Biophysical Research Communications·Hai WangGe Gao

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