ArticleBiochemical and biophysical research communications2015
Mitochondrial division inhibitor 1 (mdivi-1) enhances death receptor-mediated apoptosis in human ovarian cancer cells.
Article in Biochemical and biophysical research communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 59 citations in OpenAlex.
- Mitochondria and tumorigenesis: Molecular basis and therapeutic implications.Genes & diseases · 2026Review
- Therapeutic Promise of Mitophagy in Cancer: Advancing from Small-Molecule Regulation to Nanotechnology-Enhanced Targeting Therapy.Theranostics · 2026Review
- Cancer stem cells: mitochondria signalling pathway and strategies for therapeutic interventions.Molecular biology reports · 2025Review
- Lactic acid metabolism: gynecological cancer's Achilles' heel.Discover oncology · 2025Review
- Inhibition of Mitochondrial Dynamics by Mitochondrial Division Inhibitor-1 Suppresses Cell Migration and Metastatic Markers in Colorectal Cancer HCT116 Cells.Journal of experimental pharmacology · 2025Article
- Interleukin-6 Modulation in Ovarian Cancer Necessitates a Targeted Strategy: From the Approved to Emerging Therapies.Cancers · 2024Review
- NK cell line modified to express a potent, DR5 specific variant of TRAIL, show enhanced cytotoxicity in ovarian cancer models.Heliyon · 2024Article
- An integral role of mitochondrial function in the pathophysiology of preeclampsia.Molecular biology reports · 2024Review
- Prognostic value and immune regulatory role of dynamin 1-like in lung adenocarcinoma.Translational lung cancer research · 2023Article
- Mitophagy: A novel perspective for insighting into cancer and cancer treatment.Cell proliferation · 2022Review
- Updates on the Pivotal Roles of Mitochondria in Urothelial Carcinoma.Biomedicines · 2022Review
- Oxidative stress-mediated mitochondrial fission promotes hepatic stellate cell activation via stimulating oxidative phosphorylation.Cell death & disease · 2022Article
- The Role of Mitochondrial Dynamic Dysfunction in Age-Associated Type 2 Diabetes.The world journal of men's health · 2022Review
- Review
- Autophagy-competent mitochondrial translation elongation factor TUFM inhibits caspase-8-mediated apoptosis.Cell death and differentiation · 2022Article
- Mitochondrial quality control in the brain: The physiological and pathological roles.Frontiers in neuroscience · 2022Review
- Article
- Review
- Article
- Mdivi-1 induces spindle abnormalities and augments taxol cytotoxicity in MDA-MB-231 cells.Cell death discovery · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) based strategy is a promising targeted therapeutic approach for the treatment of a variety of cancers including ovarian cancer. However, the inherent or acquired resistance of tumor cells to TRAIL limits the potential application of TRAIL-mediated therapy. In this study, we identified that mitochondrial division inhibitor-1 (mdivi-1) is able to enhance the sensitivity of human ovarian cancer cells to death receptor ligands including TRAIL, FAS ligands, and TNF-α. Importantly, the combination of TRAIL and mdivi-1 has no apparent cytotoxic effect on non-transformed human cells, indicating a significant therapeutic window. We identified that caspase-8 and not the modulation of TRAIL receptors is required for the combination effect of TRAIL and mdivi-1. We further demonstrated that the enhanced efficacy of combination of mdivi-1 and death ligands is not dependent on the originally reported target of mdivi-1, Drp1, and is also not dependent on the two important pro-apoptotic Bcl-2 family proteins Bax and Bak. Thus, our study presents a novel strategy in enhancing the apoptotic effect of death receptor ligands and provides a new effective TRAIL-based combination approach for treating human ovarian cancer.
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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.