Synthetic lethal screening identifies compounds activating iron-dependent, nonapoptotic cell death in oncogenic-RAS-harboring cancer cells.

By W. Yang, Brent R. Stockwell. Chemistry and Biology, 2008

1,692 citations recorded by the source corpus.

Subfields: Molecular Biology, Nutrition and Dietetics, Oncology

View Paper: https://www.semanticscholar.org/paper/281328eff11f39ff40057939d59eefc0c4258aa8

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Citations in the corpus

Ferroptosis: mechanisms and links with diseases (2021, background): “, ferric ammonium citrate) enhances ferroptosis.(1,7) Several studies have shown that the regulation of genes related to iron metabolism can also regulate ferroptotic cell death, such as transferrin, nitrogen fixation 1 (NFS1), iron response element-binding protein 2 (IREB2), Nuclear receptor coacti”
Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease. (2017, positive): “Notably, transferrin and transferrin receptor, which import iron from the extracellular environment, are required for ferroptosis (Gao et al., 2015; Yang and Stockwell, 2008), while silencing of the iron metabolism master regulator IREB2 decreases sensitivity to ferroptosis (Dixon, 2012).”
Regulated cell death (RCD) in cancer: key pathways and targeted therapies (2022, background): “Studies have shown that intracellular iron overload can be prevented by knocking out the transferrin receptor (TFRC) on the cell surface, or the storage of iron in the inert pool can be increased by upregulating cytoplasmic ferritin to inhibit the occurrence of ferroptosis.(380) Similarly, inhibitin”
Multi-stage differentiation defines melanoma subtypes with differential vulnerability to drug-induced iron-dependent oxidative stress (2018, background): “See also Figure S6. dependence on MAPK signaling for ferroptosis in some contexts (Yang and Stockwell, 2008; Yagoda et al., 2007).”
Transferrin Receptor Is a Specific Ferroptosis Marker (2020, neutral): “It was reported previously that cells with knockdown of TfR1 became more resistant to erastin-induced cell death (Yang and Stockwell, 2008) and that siTfR1 RNAi significantly inhibited serum-dependent necrosis, which was subsequently determined to be ferroptosis (Gao et al.”
Regulation of Ferroptotic Cancer Cell Death by GPX4 (2014, background): “We have reported the identification of additional small molecules, named RSL3 (Yang and Stockwell, 2008a), ML162, and DPI10 (Weı̈wer et al., 2012), that display oncogenic-RASsynthetic-lethality (the RSL phenotype) in engineered fibroblast-derived tumorigenic cell lines.”
Oxidative Stress in Cancer (2020, background): “Evidence suggests that GPX4 and maintenance of intracellular cysteine levels are each important in suppressing ferroptosis as the GPX4 inhibitor RSL-3, and the cystine/glutamate antiporter xCT inhibitor erastin, can markedly stimulate death in cancer cells harboring oncogenic RAS (Yang and Stockwell”