ArticleOncotarget2015
Inhibition of Lon protease by triterpenoids alters mitochondria and is associated to cell death in human cancer cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 70 citations in OpenAlex.
- Direct coupling and protective activation of DRP1 by the DNA-PKcs inhibitor KU-57788 synergizes with ferroptosis in anaplastic thyroid cancer cells.Cell death & disease · 2026Article
- Molecular mechanisms of mitochondrial AAA+ proteases.The Journal of biological chemistry · 2026Review
- Dual targeting of the mitochondrial Lon peptidase 1 and the chymotrypsin-like proteasome activity as a potential therapeutic strategy in malignant astrocytoma models.Pharmacological research · 2025Article
- The mitochondrial LONP1 protease: molecular targets and role in pathophysiology.Molecular biology reports · 2025Review
- Modulation of Lonp1 Activity by Small Compounds.Biomolecules · 2025Review
- The synthetic oleanane triterpenoid CDDO-2P-Im binds GRP78/BiP to induce unfolded protein response-mediated apoptosis in myeloma.Molecular oncology · 2023Article
- Mitochondria Deregulations in Cancer Offer Several Potential Targets of Therapeutic Interventions.International journal of molecular sciences · 2023Review
- Glucocerebrosidase is imported into mitochondria and preserves complex I integrity and energy metabolism.Nature communications · 2023Article
- Respiratory Complex I dysfunction in cancer: from a maze of cellular adaptive responses to potential therapeutic strategies.The FEBS journal · 2022Review
- Roles of LonP1 in Oral-Maxillofacial Developmental Defects and Tumors: A Novel Insight.International journal of molecular sciences · 2022Review
- Mitochondrial oxidative stress in the tumor microenvironment and cancer immunoescape: foe or friend?Journal of biomedical science · 2022Review
- Evidence for mitochondrial Lonp1 expression in the nucleus.Scientific reports · 2022Article
- Flow Cytometric Analysis of Oxidative Stress inInternational journal of molecular sciences · 2022Article
- Posttranslational regulation of mitochondrial frataxin and identification of compounds that increase frataxin levels in Friedreich's ataxia.The Journal of biological chemistry · 2022Article
- Novel Soloxolone Amides as Potent Anti-Glioblastoma Candidates: Design, Synthesis, In Silico Analysis and Biological Activities In Vitro and In Vivo.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Organismal and Cellular Stress Responses upon Disruption of Mitochondrial Lonp1 Protease.Cells · 2022Article
- Inhibition of mitochondrial LonP1 protease by allosteric blockade of ATP binding and hydrolysis via CDDO and its derivatives.The Journal of biological chemistry · 2022Article
- Insight into the mitochondrial unfolded protein response and cancer: opportunities and challenges.Cell & bioscience · 2022Review
- Mitochondrial ATP-Dependent Proteases-Biological Function and Potential Anti-Cancer Targets.Cancers · 2021Review
- Targeting Mitochondrial Protein Expression as a Future Approach for Cancer Therapy.Frontiers in oncology · 2021Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial Lon protease (Lon) regulates several mitochondrial functions, and is inhibited by the anticancer molecule triterpenoid 2-cyano-3, 12-dioxooleana-1,9(11)-dien-28-oic acid (CDDO), or by its C-28 methyl ester derivative (CDDO-Me). To analyze the mechanism of action of triterpenoids, we investigated intramitochondrial reactive oxygen species (ROS), mitochondrial membrane potential, mitochondrial mass, mitochondrial dynamics and morphology, and Lon proteolytic activity in RKO human colon cancer cells, in HepG2 hepatocarcinoma cells and in MCF7 breast carcinoma cells. We found that CDDO and CDDO-Me are potent stressors for mitochondria in cancer cells, rather than normal non-transformed cells. In particular, they: i) cause depolarization; ii) increase mitochondrial ROS, iii) alter mitochondrial morphology and proteins involved in mitochondrial dynamics; iv) affect the levels of Lon and those of aconitase and human transcription factor A, which are targets of Lon activity; v) increase level of protein carbonyls in mitochondria; vi) lead to intrinsic apoptosis. The overexpression of Lon can rescue cells from cell death, providing an additional evidence on the role of Lon in conditions of excessive stress load.
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