ArticleEuropean journal of medical research2014
The roles of mitoferrin-2 in the process of arsenic trioxide-induced cell damage in human gliomas.
Article in European journal of medical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Review
- Mitoferrin-1 Promotes Proliferation and Abrogates Protein Oxidation via the Glutathione Pathway in Glioblastoma.Antioxidants (Basel, Switzerland) · 2023Article
- Review
- The Emerging Role of RNA N6-Methyladenosine Modification in Pancreatic Cancer.Frontiers in oncology · 2022Review
- Identification of Iron Metabolism-Related Gene Signatures for Predicting the Prognosis of Patients With Sarcomas.Frontiers in oncology · 2020Article
- Arsenic trioxide as a novel anti-glioma drug: a review.Cellular & molecular biology letters · 2020Review
- Mitochondrial Iron in Human Health and Disease.Annual review of physiology · 2019Review
- Arsenic trioxide induces apoptosis and the formation of reactive oxygen species in rat glioma cells.Cellular & molecular biology letters · 2018Article
- Arsenic trioxide inhibits glioma cell growth through induction of telomerase displacement and telomere dysfunction.Oncotarget · 2016Article
- Impact of Mitochondria-Mediated Apoptosis in U251 Cell Cycle Arrest in G1 Stage and Caspase Activation.Medical science monitor : international medical journal of experimental and clinical research · 2015Article
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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
backgroundAmong glioma treatment strategies, arsenic trioxide (As2O3) has shown efficacy as a therapeutic agent against human gliomas. However, the exact antitumor mechanism of action of As2O3 is still unclear. Mitochondria are considered to be the major source of intracellular reactive oxygen species (ROS), which are known to be associated with As2O3-induced cell damage. Therefore, we investigated whether mitoferrin-2, a mitochondrial iron uptake transporter, participates in As2O3-induced cell killing in human gliomas.
methodsHuman glioma cell lines were used to explore the mechanism of As2O3's antitumor effects. First, expression of mitoferrin-2 was analyzed in glioma cells that were pretreated with As2O3. Changes in ROS production and apoptosis were assessed. Furthermore, cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT).
resultsIn the present study we found that As2O3 induced ROS production and apoptosis in glioma cells. In addition, gene expression of mitoferrin-2, a mitochondrial iron uptake transporter, was increased 4 to 5 fold after exposure to As2O3 (5 μM) for 48 hours. Furthermore, apoptosis and cytotoxicity induced by As2O3 in glioma cells were decreased after silencing the mitoferrin-2 gene.
conclusionsOur findings indicated that mitoferrin-2 participates in mitochondrial ROS-dependent mechanisms underlying As2O3-mediated damage in glioma cells.
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