{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["23(1)"],"submitter":["Nandha SR"],"pubmed_abstract":["<h4>Background</h4>Cancer cells, which rely heavily on mitochondria for their energy demands and oncometabolites, have a high mitochondrial load, often associated with an aggressive, invasive, and metastatic phenotype. Mitochondrial ROS (mtROS), which play a causal role in cancer, represent the Achilles' heel of cancer since excessive mtROS causes protein misfolding/aggregation, resulting in cell death via proteotoxic stress. Furthermore, the detailed underlying mechanism(s) of mitochondrial oxidative stress-induced cell death remain obscure.<h4>Methods</h4>Cell growth was estimated by MTT assay, clonogenic assay, live-cell imaging and flow cytometry. Intracellular ROS, mtROS, glutathione and antioxidant levels were studied by spectrophotometry. RNAseq and Western blotting were performed t"],"journal":["Cell communication and signaling : CCS"],"pagination":["393"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12406427"],"repository":["biostudies-literature"],"pubmed_title":["Targeting mitochondrial proteases CLPP and LONP1 via disruption of mitochondrial redox homeostasis induces proteotoxic stress and suppresses tumor progression."],"pmcid":["PMC12406427"],"pubmed_authors":["Patwardhan RS","Sharma D","Nandha SR","Checker R","Sandur SK"],"additional_accession":[]},"is_claimable":false,"name":"Targeting mitochondrial proteases CLPP and LONP1 via disruption of mitochondrial redox homeostasis induces proteotoxic stress and suppresses tumor progression.","description":"<h4>Background</h4>Cancer cells, which rely heavily on mitochondria for their energy demands and oncometabolites, have a high mitochondrial load, often associated with an aggressive, invasive, and metastatic phenotype. Mitochondrial ROS (mtROS), which play a causal role in cancer, represent the Achilles' heel of cancer since excessive mtROS causes protein misfolding/aggregation, resulting in cell death via proteotoxic stress. Furthermore, the detailed underlying mechanism(s) of mitochondrial oxidative stress-induced cell death remain obscure.<h4>Methods</h4>Cell growth was estimated by MTT assay, clonogenic assay, live-cell imaging and flow cytometry. Intracellular ROS, mtROS, glutathione and antioxidant levels were studied by spectrophotometry. RNAseq and Western blotting were performed t","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-04-08T16:11:07.608Z","creation":"2026-04-08T06:11:12.367Z"},"accession":"S-EPMC12406427","cross_references":{"pubmed":["40903791"],"doi":["10.1186/s12964-025-02127-w"]}}