{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Pan Z"],"funding":["National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["31"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12371041"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(1)"],"pubmed_abstract":["Antipsychotic drugs have been shown to suppress tumor growth and induce cell death, but their clinical application remains limited. Pimozide, an FDA-approved antipsychotic, holds significant potential for cancer treatment. However, the mechanisms underlying tumor cell responses to Pimozide remain unclear. In this study, we identify a critical role for peroxisomes in mediating tumor cell resistance to Pimozide. Our findings demonstrate that Pimozide increases peroxisome numbers and that peroxisomal deficiency significantly enhances Pimozide-induced cell death. We show that peroxisomes mitigate Pimozide-induced apoptosis primarily through fatty acid oxidation and ether lipid synthesis, rather than reactive oxygen species (ROS) metabolism. Moreover, Pimozide treatment upregulates peroxisomal "],"journal":["Oncogenesis"],"pubmed_title":["Peroxisomal lipid metabolism inhibits Pimozide-induced cancer cell death by regulating ATP homeostasis."],"pmcid":["PMC12371041"],"funding_grant_id":["32170736","32370776"],"pubmed_authors":["Pan Z","Yang Z","Guo J","Li F","Yu F","Cui F","You W"],"additional_accession":[]},"is_claimable":false,"name":"Peroxisomal lipid metabolism inhibits Pimozide-induced cancer cell death by regulating ATP homeostasis.","description":"Antipsychotic drugs have been shown to suppress tumor growth and induce cell death, but their clinical application remains limited. Pimozide, an FDA-approved antipsychotic, holds significant potential for cancer treatment. However, the mechanisms underlying tumor cell responses to Pimozide remain unclear. In this study, we identify a critical role for peroxisomes in mediating tumor cell resistance to Pimozide. Our findings demonstrate that Pimozide increases peroxisome numbers and that peroxisomal deficiency significantly enhances Pimozide-induced cell death. We show that peroxisomes mitigate Pimozide-induced apoptosis primarily through fatty acid oxidation and ether lipid synthesis, rather than reactive oxygen species (ROS) metabolism. Moreover, Pimozide treatment upregulates peroxisomal ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Aug","modification":"2026-05-09T10:47:29.708Z","creation":"2026-04-08T00:48:10.883Z"},"accession":"S-EPMC12371041","cross_references":{"pubmed":["40841534"],"doi":["10.1038/s41389-025-00575-0"]}}