ArticleJournal of experimental & clinical cancer research : CR2015
ROS-p53-cyclophilin-D signaling mediates salinomycin-induced glioma cell necrosis.
Article in Journal of experimental & clinical cancer research : CR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 109 citations in OpenAlex.
- miR-125b Attenuates Sepsis-Induced Hippocampal Mitochondrial Fission and Cognitive Impairment via the ROS/p53 Pathway.Molecular neurobiology · 2026Article
- Development of a Mitochondrial Permeability Transition-Driven Necrosis-Related Prognostic Signature in Cervical Cancer: Integrating Bulk Transcriptomic and Single-Cell Data.Cancer medicine · 2025Article
- p53-regulated non-apoptotic cell death pathways and their relevance in cancer and other diseases.Nature reviews. Molecular cell biology · 2025Review
- Valproic Acid Reduces Invasiveness and Cellular Growth in 2D and 3D Glioblastoma Cell Lines.International journal of molecular sciences · 2025Article
- Ultrasound-responsive nanoparticles for imaging and therapy of brain tumors.Materials today. Bio · 2025Review
- The interplay of mitochondrial dysfunction and altered metabolic pathways in glioblastoma.Contemporary oncology (Poznan, Poland) · 2025Review
- Ultrastructural changes in cardiac and skeletal myoblasts following in vitro exposure to monensin, salinomycin, and lasalocid.PloS one · 2024Article
- Neuron-secreted NLGN3 ameliorates ischemic brain injury via activating Gαi1/3-Akt signaling.Cell death & disease · 2023Article
- ROS regulation in gliomas: implications for treatment strategies.Frontiers in immunology · 2023Review
- Cyclophilin A/CD147 Interaction: A Promising Target for Anticancer Therapy.International journal of molecular sciences · 2022Review
- Nrf2 signaling activation by a small molecule activator compound 16 inhibits hydrogen peroxide-induced oxidative injury and death in osteoblasts.Cell death discovery · 2022Article
- The synergistic anticancer effect of salinomycin combined with cabazitaxel in CD44+ prostate cancer cells by downregulating wnt, NF-κB and AKT signaling.Molecular biology reports · 2022Article
- Salinomycin as a potent anticancer stem cell agent: State of the art and future directions.Medicinal research reviews · 2022Review
- Synergistic inhibition of the growth of MDA-MB-231 cells in triple-negative breast cancer by salinomycin combined with 17-AAG and its mechanism.Oncology letters · 2022Article
- GNE-493 inhibits prostate cancer cell growth via Akt-mTOR-dependent and -independent mechanisms.Cell death discovery · 2022Article
- Cyclophilin D: Guardian or Executioner for Tumor Cells?Frontiers in oncology · 2022Review
- Immune regulation and emerging roles of noncoding RNAs inFrontiers in immunology · 2022Review
- The sphingosine kinase inhibitor SKI-V suppresses cervical cancer cell growth.International journal of biological sciences · 2022Article
- G-protein-coupled receptor GPR17 inhibits glioma development by increasing polycomb repressive complex 1-mediated ROS production.Cell death & disease · 2021Article
- MAFG-driven osteosarcoma cell progression is inhibited by a novel miRNA miR-4660.Molecular therapy. Nucleic acids · 2021Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe primary glioblastoma multiforme (GBM) is the most malignant form of astrocytic tumor with an average survival of approximately 12-14 months. The search for novel and more efficient chemo-agents against this disease is urgent. Salinomycin induces broad anti-cancer effects; however, its role in GBM and the underlying mechanism are not clear.
resultsHere we found that salinomycin induced both apoptosis and necrosis in cultured glioma cells, and necrosis played a major role in contributing salinomycin's cytotoxicity. Salinomycin induced p53 translocation to mitochondria, where it formed a complex with cyclophilin-D (CyPD). This complexation was required for mitochondrial permeability transition pore (mPTP) opening and subsequent programmed necrosis. Blockade of Cyp-D by siRNA-mediated depletion or pharmacological inhibitors (cyclosporin A and sanglifehrin A) significantly suppressed salinomycin-induced glioma cell necrosis. Meanwhile, p53 stable knockdown alleviated salinomycin-induced necrosis in glioma cells. Reactive oxygen species (ROS) production was required for salinomycin-induced p53 mitochondrial translocation, mPTP opening and necrosis, and anti-oxidants n-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC) inhibited p53 translocation, mPTP opening and glioma cell death.
conclusionsThus, salinomycin mainly induces programmed necrosis in cultured glioma cells.
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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.