ArticleOncotarget2015
Distinct effects of TRAIL on the mitochondrial network in human cancer cells and normal cells: role of plasma membrane depolarization.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 53 citations in OpenAlex.
- Preclinical Evaluation of Labetalol for Cutaneous Melanoma Drug Repurposing: Cytotoxic Activity in A375 Cells and Mitochondria-Associated Apoptotic Signaling.Medicina (Kaunas, Lithuania) · 2026Article
- Unlocking mitochondrial dysfunction-associated senescence (MiDAS) with NADTranslational oncology · 2024Article
- Enhanced anti-tumor efficacy with multi-transgene armed mesenchymal stem cells for treating peritoneal carcinomatosis.Journal of translational medicine · 2024Article
- Mitochondrial Dynamin-Related Protein Drp1: a New Player in Cardio-oncology.Current oncology reports · 2022Review
- Oxidative stress-mediated mitochondrial fission promotes hepatic stellate cell activation via stimulating oxidative phosphorylation.Cell death & disease · 2022Article
- Mitochondrial fission induces immunoescape in solid tumors through decreasing MHC-I surface expression.Nature communications · 2022Article
- Astaxanthin Sensitizes Low SOD2-Expressing GBM Cell Lines to TRAIL Treatment via Pathway Involving Mitochondrial Membrane Depolarization.Antioxidants (Basel, Switzerland) · 2022Article
- Air Plasma-Activated Medium Evokes a Death-Associated Perinuclear Mitochondrial Clustering.International journal of molecular sciences · 2022Article
- Article
- Aspirin Induces Mitochondrial CaInternational journal of molecular sciences · 2020Article
- Molecular and Clinical Relevance ofCancers · 2020Article
- Article
- Role of Mitochondria in Cancer Immune Evasion and Potential Therapeutic Approaches.Frontiers in immunology · 2020Review
- Autophagy inhibitors regulate TRAIL sensitivity in human malignant cells by targeting the mitochondrial network and calcium dynamics.International journal of oncology · 2019Article
- Methylene Blue-Mediated Photodynamic Therapy Induces Macrophage Apoptosis via ROS and Reduces Bone Resorption in Periodontitis.Oxidative medicine and cellular longevity · 2019Article
- Verteporfin suppresses the proliferation, epithelial-mesenchymal transition and stemness of head and neck squamous carcinoma cells via inhibiting YAP1.Journal of Cancer · 2019Article
- MicroRNA-668 represses MTP18 to preserve mitochondrial dynamics in ischemic acute kidney injury.The Journal of clinical investigation · 2018Article
- Cold PSM, but not TRAIL, triggers autophagic cell death: A therapeutic advantage of PSM over TRAIL.International journal of oncology · 2018Article
- Plasma-stimulated medium kills TRAIL-resistant human malignant cells by promoting caspase-independent cell death via membrane potential and calcium dynamics modulation.International journal of oncology · 2018Article
- Mitochondrial Dynamics in Type 2 Diabetes and Cancer.Frontiers in endocrinology · 2018Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apo2 ligand/tumor necrosis factor-related apoptosis-inducing ligand (Apo2L/TRAIL) is a promising anticancer drug due to its tumor-selective cytotoxicity. Here we report that TRAIL exhibits distinct effects on the mitochondrial networks in malignant cells and normal cells. Live-cell imaging revealed that multiple human cancer cell lines and normal cells exhibited two different modes of mitochondrial responses in response to TRAIL and death receptor agonists. Mitochondria within tumor cells became fragmented into punctate and clustered in response to toxic stimuli. The mitochondrial fragmentation was observed at 4 h, then became more pronounced over time, and associated with apoptotic cell death. In contrast, mitochondria within normal cells such as melanocytes and fibroblasts became only modestly truncated, even when they were treated with toxic stimuli. Although TRAIL activated dynamin-related protein 1 (Drp1)-dependent mitochondrial fission, inhibition of this process by Drp1 knockdown or with the Drp1 inhibitor mdivi-1, potentiated TRAIL-induced apoptosis, mitochondrial fragmentation, and clustering. Moreover, mitochondrial reactive oxygen species (ROS)-mediated depolarization accelerated mitochondrial network abnormalities in tumor cells, but not in normal cells, and TRAIL caused higher levels of mitochondrial ROS accumulation and depolarization in malignant cells than in normal cells. Our findings suggest that tumor cells are more prone than normal cells to oxidative stress and depolarization, thereby being more vulnerable to mitochondrial network abnormalities and that this vulnerability may be relevant to the tumor-targeting killing by TRAIL.
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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.