{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Alvarez-Valadez K"],"funding":["Ligue Contre le Cancer","Cancer Research ASPIRE","INCa","Equipex Onco-Pheno-Screen","RHU Immunolife","Association pour la Recherche sur le Cancer","Institut National Du Cancer","Agence Nationale de la Recherche","Gustave Roussy Odyssea","Institut National de la Santé et de la Recherche Médicale","LabEx Immuno-Oncology","Institut Universitaire de France","Fondation Carrefour","Cancéropôle Ile-de-France","European Union Horizon 2020 Projects Oncobiome and Crimson","Seerave Foundation","SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination","SIRIC Cancer Research and Personalized Medicine","IdEx Université de Paris","European Joint Programme on Rare Diseases","Fondation pour la Recherche Médicale","Taxe d’apprentissage","Consejo Nacional de Ciencia y Tecnología de México"],"pagination":["934-956"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12013445"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(5)"],"pubmed_abstract":["Cholesterol serves as a vital lipid that regulates numerous physiological processes. Nonetheless, its role in regulating cell death processes remains incompletely understood. In this study, we investigated the role of cholesterol trafficking in immunogenic cell death. Through cell-based drug screening, we identified two antidepressants, sertraline and indatraline, as potent inducers of the nuclear translocation of TFEB (transcription factor EB). Activation of TFEB was mediated through the autophagy-independent lipidation of MAP1LC3/LC3 (microtubule associated protein 1 light chain 3). Both compounds promoted cholesterol accumulation within lysosomes, resulting in lysosomal membrane permeabilization, disruption of autophagy and cell death that could be reversed by cholesterol depletion. Mol"],"journal":["Autophagy"],"pubmed_title":["Lysosomal damage due to cholesterol accumulation triggers immunogenic cell death."],"pmcid":["PMC12013445"],"funding_grant_id":["ANR-18-IDEX-0001","757821","PLBIO23–216","AMMICA US23/CNRS UMS3655","ANR-19-CE15-0013","IP/SC-17519","ANR-21-CE44-0016","IGR KAAL-2022","ANR-23-CE13-0013-0","PLBIO22–101"],"pubmed_authors":["Wodrich H","Pol JG","Lambertucci F","de Brevern AG","Kroemer G","Diharce J","Leduc M","Forveille S","Maiuri MC","Guittat L","Sauvat A","Stoll G","Muller A","Kepp O","Djavaheri-Mergny M","Alvarez-Valadez K","Motino O","Ferret L","Paillet J"],"additional_accession":[]},"is_claimable":false,"name":"Lysosomal damage due to cholesterol accumulation triggers immunogenic cell death.","description":"Cholesterol serves as a vital lipid that regulates numerous physiological processes. Nonetheless, its role in regulating cell death processes remains incompletely understood. In this study, we investigated the role of cholesterol trafficking in immunogenic cell death. Through cell-based drug screening, we identified two antidepressants, sertraline and indatraline, as potent inducers of the nuclear translocation of TFEB (transcription factor EB). Activation of TFEB was mediated through the autophagy-independent lipidation of MAP1LC3/LC3 (microtubule associated protein 1 light chain 3). Both compounds promoted cholesterol accumulation within lysosomes, resulting in lysosomal membrane permeabilization, disruption of autophagy and cell death that could be reversed by cholesterol depletion. Mol","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 May","modification":"2026-06-06T15:04:26.314Z","creation":"2026-06-01T03:10:34.043Z"},"accession":"S-EPMC12013445","cross_references":{"pubmed":["39663580"],"doi":["10.1080/15548627.2024.2440842"]}}