{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wu K"],"funding":["NCRR NIH HHS","NCI NIH HHS","NIH HHS","NIGMS NIH HHS"],"pagination":["487-495"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12779550"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["649(8096)"],"pubmed_abstract":["Emerging evidence indicates that cancer cells are susceptible to ferroptosis, a form of cell death that is triggered by uncontrolled lipid peroxidation<sup>1-3</sup>. Despite broad enthusiasm about harnessing ferroptosis as a novel anti-cancer strategy, whether ferroptosis is a barrier to tumorigenesis and can be leveraged therapeutically remains unknown<sup>4,5</sup>. Here, using genetically engineered mouse models of lung adenocarcinoma, we performed tumour-specific loss-of-function studies of two key ferroptosis suppressors, GPX4<sup>6,7</sup> and ferroptosis suppressor protein 1 (FSP1)<sup>8,9</sup>, and observed increased lipid peroxidation and robust suppression of tumorigenesis, suggesting that lung tumours are highly sensitive to ferroptosis. Furthermore, across multiple pre-clinic"],"journal":["Nature"],"pubmed_title":["Targeting FSP1 triggers ferroptosis in lung cancer."],"pmcid":["PMC12779550"],"funding_grant_id":["S10 RR027926","P30 CA016087","R01 CA262562","R37 CA222504","T32 GM136573","S10 OD021747","R01 CA227649","S10 OD032292","T32 GM136542","R01 CA283049","F30 CA275258"],"pubmed_authors":["Wu K","Papagiannakopoulos T","Bossowski JP","Chung S","Pillai R","Han M","Simeone D","Hao Y","Conrad M","Ziogou A","Wang L","Kim TH","Nakamura MN","Vaughan AJ","Mancini M","Rajalingam S","Nakamura T","Shackelford D","Kim SM","Kang YP"],"additional_accession":[]},"is_claimable":false,"name":"Targeting FSP1 triggers ferroptosis in lung cancer.","description":"Emerging evidence indicates that cancer cells are susceptible to ferroptosis, a form of cell death that is triggered by uncontrolled lipid peroxidation<sup>1-3</sup>. Despite broad enthusiasm about harnessing ferroptosis as a novel anti-cancer strategy, whether ferroptosis is a barrier to tumorigenesis and can be leveraged therapeutically remains unknown<sup>4,5</sup>. Here, using genetically engineered mouse models of lung adenocarcinoma, we performed tumour-specific loss-of-function studies of two key ferroptosis suppressors, GPX4<sup>6,7</sup> and ferroptosis suppressor protein 1 (FSP1)<sup>8,9</sup>, and observed increased lipid peroxidation and robust suppression of tumorigenesis, suggesting that lung tumours are highly sensitive to ferroptosis. Furthermore, across multiple pre-clinic","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan","modification":"2026-06-06T12:54:56.098Z","creation":"2026-05-30T03:11:38.886Z"},"accession":"S-EPMC12779550","cross_references":{"pubmed":["41193800"],"doi":["10.1038/s41586-025-09710-8"]}}