ArticleJournal of cellular physiology2013
Mitochondrial-targeted nitroxides disrupt mitochondrial architecture and inhibit expression of peroxiredoxin 3 and FOXM1 in malignant mesothelioma cells.
Article in Journal of cellular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- Preclinical characterization and phase 1 clinical testing of targeting mitochondrial peroxiredoxin 3 in cancer.Nature communications · 2026Article
- Up-regulation of peroxiredoxin 3 by high-risk human papillomavirus in cervical cancer cells.Archives of medical science : AMS · 2026Article
- Inhibition of Mitochondrial Antioxidant Defense and CDK4/6 in Mesothelioma.Molecules (Basel, Switzerland) · 2023Article
- Oxidative stress-mediated mitochondrial fission promotes hepatic stellate cell activation via stimulating oxidative phosphorylation.Cell death & disease · 2022Article
- Article
- Motor proteins at the mitochondria-cytoskeleton interface.Journal of cell science · 2021Review
- RETRACTED: Identification of Redox-Sensitive Transcription Factors as Markers of Malignant Pleural Mesothelioma.Cancers · 2021Article
- Unique Cellular and Biochemical Features of Human Mitochondrial Peroxiredoxin 3 Establish the Molecular Basis for Its Specific Reaction with Thiostrepton.Antioxidants (Basel, Switzerland) · 2021Article
- Mitochondrial Fission Protein 1: Emerging Roles in Organellar Form and Function in Health and Disease.Frontiers in endocrinology · 2021Review
- FOXM1 nuclear transcription factor translocates into mitochondria and inhibits oxidative phosphorylation.Molecular biology of the cell · 2020Article
- Peroxiredoxins and Beyond; Redox Systems Regulating Lung Physiology and Disease.Antioxidants & redox signaling · 2019Review
- Mitochondria-targeted drugs stimulate mitophagy and abrogate colon cancer cell proliferation.The Journal of biological chemistry · 2018Article
- Detection of mitochondria-generated reactive oxygen species in cells using multiple probes and methods: Potentials, pitfalls, and the future.The Journal of biological chemistry · 2018Article
- Teaching the basics of reactive oxygen species and their relevance to cancer biology: Mitochondrial reactive oxygen species detection, redox signaling, and targeted therapies.Redox biology · 2018Review
- Hyperoxia Causes Mitochondrial Fragmentation in Pulmonary Endothelial Cells by Increasing Expression of Pro-Fission Proteins.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Mitochondrial dysfunction activates lysosomal-dependent mitophagy selectively in cancer cells.Oncotarget · 2018Article
- Nanopreparations for mitochondria targeting drug delivery system: Current strategies and future prospective.Asian journal of pharmaceutical sciences · 2017Review
- To mdivi-1 or not to mdivi-1: Is that the question?Developmental neurobiology · 2017Review
- Mitochondria-Targeted Triphenylphosphonium-Based Compounds: Syntheses, Mechanisms of Action, and Therapeutic and Diagnostic Applications.Chemical reviews · 2017Review
- AMPK activity regulates trafficking of mitochondria to the leading edge during cell migration and matrix invasion.Molecular biology of the cell · 2016Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Malignant mesothelioma (MM) is an intractable tumor of the peritoneal and pleural cavities primarily linked to exposure to asbestos. Recently, we described an interplay between mitochondrial-derived oxidants and expression of FOXM1, a redox-responsive transcription factor that has emerged as a promising therapeutic target in solid malignancies. Here we have investigated the effects of nitroxides targeted to mitochondria via triphenylphosphonium (TPP) moieties on mitochondrial oxidant production, expression of FOXM1 and peroxiredoxin 3 (PRX3), and cell viability in MM cells in culture. Both Mito-carboxy-proxyl (MCP) and Mito-TEMPOL (MT) caused dose-dependent increases in mitochondrial oxidant production that was accompanied by inhibition of expression of FOXM1 and PRX3 and loss of cell viability. At equivalent concentrations TPP, CP, and TEMPOL had no effect on these endpoints. Live cell ratiometric imaging with a redox-responsive green fluorescent protein targeted to mitochondria (mito-roGFP) showed that MCP and MT, but not CP, TEMPOL, or TPP, rapidly induced mitochondrial fragmentation and swelling, morphological transitions that were associated with diminished ATP levels and increased production of mitochondrial oxidants. Mdivi-1, an inhibitor of mitochondrial fission, did not rescue mitochondria from fragmentation by MCP. Immunofluorescence microscopy experiments indicate a fraction of FOXM1 coexists in the cytoplasm with mitochondrial PRX3. Our results indicate that MCP and MT inhibit FOXM1 expression and MM tumor cell viability via perturbations in redox homeostasis caused by marked disruption of mitochondrial architecture, and suggest that both compounds, either alone or in combination with thiostrepton or other agents, may provide credible therapeutic options for the management of MM.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.