<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>23(1)</volume><submitter>Nandha SR</submitter><pubmed_abstract>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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</pubmed_abstract><journal>Cell communication and signaling : CCS</journal><pagination>393</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12406427</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Targeting mitochondrial proteases CLPP and LONP1 via disruption of mitochondrial redox homeostasis induces proteotoxic stress and suppresses tumor progression.</pubmed_title><pmcid>PMC12406427</pmcid><pubmed_authors>Patwardhan RS</pubmed_authors><pubmed_authors>Sharma D</pubmed_authors><pubmed_authors>Nandha SR</pubmed_authors><pubmed_authors>Checker R</pubmed_authors><pubmed_authors>Sandur SK</pubmed_authors></additional><is_claimable>false</is_claimable><name>Targeting mitochondrial proteases CLPP and LONP1 via disruption of mitochondrial redox homeostasis induces proteotoxic stress and suppresses tumor progression.</name><description>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Sep</publication><modification>2026-04-08T16:11:07.608Z</modification><creation>2026-04-08T06:11:12.367Z</creation></dates><accession>S-EPMC12406427</accession><cross_references><pubmed>40903791</pubmed><doi>10.1186/s12964-025-02127-w</doi></cross_references></HashMap>