{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yang X"],"funding":["NIAID NIH HHS","NCI NIH HHS","NINDS NIH HHS"],"pagination":["762-777.e9"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11209835"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["36(4)"],"pubmed_abstract":["Although the role of ferroptosis in killing tumor cells is well established, recent studies indicate that ferroptosis inducers also sabotage anti-tumor immunity by killing neutrophils and thus unexpectedly stimulate tumor growth, raising a serious issue about whether ferroptosis effectively suppresses tumor development in vivo. Through genome-wide CRISPR-Cas9 screenings, we discover a pleckstrin homology-like domain family A member 2 (PHLDA2)-mediated ferroptosis pathway that is neither ACSL4-dependent nor requires common ferroptosis inducers. PHLDA2-mediated ferroptosis acts through the peroxidation of phosphatidic acid (PA) upon high levels of reactive oxygen species (ROS). ROS-induced ferroptosis is critical for tumor growth in the absence of common ferroptosis inducers; strikingly, los"],"journal":["Cell metabolism"],"pubmed_title":["PHLDA2-mediated phosphatidic acid peroxidation triggers a distinct ferroptotic response during tumor suppression."],"pmcid":["PMC11209835"],"funding_grant_id":["R01 CA258390","P30 CA008748","R01 CA243142","R37 NS061817","R01 CA266342","R01 CA166413","R35 CA209896","R01 CA258622","P30 CA013696","R01 CA204232","R01 CA165065","R01 CA254970","U01 AI156923","U01 AI156924","R01 NS076511","R01 NS061817","R35 CA253059"],"pubmed_authors":["Stockwell BR","Gu W","Kon N","Chen D","Tycko B","Yang X","Bayir H","Kagan VE","Kapralov AA","Li Z","Zhang Z","Jiang X","Amoscato AA","Duan S","Tyurin VA","Wang Z","Samovich SN","Dar HH"],"additional_accession":[]},"is_claimable":false,"name":"PHLDA2-mediated phosphatidic acid peroxidation triggers a distinct ferroptotic response during tumor suppression.","description":"Although the role of ferroptosis in killing tumor cells is well established, recent studies indicate that ferroptosis inducers also sabotage anti-tumor immunity by killing neutrophils and thus unexpectedly stimulate tumor growth, raising a serious issue about whether ferroptosis effectively suppresses tumor development in vivo. Through genome-wide CRISPR-Cas9 screenings, we discover a pleckstrin homology-like domain family A member 2 (PHLDA2)-mediated ferroptosis pathway that is neither ACSL4-dependent nor requires common ferroptosis inducers. PHLDA2-mediated ferroptosis acts through the peroxidation of phosphatidic acid (PA) upon high levels of reactive oxygen species (ROS). ROS-induced ferroptosis is critical for tumor growth in the absence of common ferroptosis inducers; strikingly, los","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Apr","modification":"2026-05-29T10:04:40.328Z","creation":"2025-04-07T02:10:30.589Z"},"accession":"S-EPMC11209835","cross_references":{"pubmed":["38309267"],"doi":["10.1016/j.cmet.2024.01.006"]}}