ArticleInternational journal of nanomedicine2018
Silica nanoparticle-induced oxidative stress and mitochondrial damage is followed by activation of intrinsic apoptosis pathway in glioblastoma cells.
Article in International journal of nanomedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 91 citations in OpenAlex.
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- Mitochondrial antioxidant enzyme (SOD2) at the crossroads of redox signaling and cancer progression.Free radical research · 2026Review
- Oleuropein- and hydroxytyrosol-loaded nanoparticles: a novel strategy against glioblastoma aggressiveness.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Silica nanoparticles trigger striatal oxidative stress, apoptosis, and histopathological alterations: in vivo and in silico molecular docking insights.Histochemistry and cell biology · 2025Article
- Diosgenin ameliorates silica-induced tuberculosis in rats.Animal models and experimental medicine · 2025Article
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- Assessing cytotoxicity and endoplasmic reticulum stress in human blood-brain barrier cells due to silver and copper oxide nanoparticles.Journal of applied genetics · 2025Article
- Design, synthesis, andRSC advances · 2024Article
- Cytotoxicity, Proapoptotic Activity and Drug-like Potential of Quercetin and Kaempferol in Glioblastoma Cells: Preclinical Insights.International journal of molecular sciences · 2024Article
- Review
- The Proteasome Inhibitor Marizomib Evokes Endoplasmic Reticulum Stress and Promotes Apoptosis in Human Glioblastoma Cells.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Applications of 3D organoids in toxicological studies: a comprehensive analysis based on bibliometrics and advances in toxicological mechanisms.Archives of toxicology · 2024Review
- Progress of nanoparticle drug delivery system for the treatment of glioma.Frontiers in bioengineering and biotechnology · 2024Review
- The Apoptosis Inhibitor Protein Survivin Is a Critical Cytoprotective Resistor against Silica-Based Nanotoxicity.Nanomaterials (Basel, Switzerland) · 2023Article
- Silica Nanoparticles Promote Apoptosis in Ovarian Granulosa Cells via Autophagy Dysfunction.International journal of molecular sciences · 2023Article
- A toxicological profile of silica nanoparticles.Toxicology research · 2022Review
- Reproductive toxicity investigation of silica nanoparticles in male pubertal mice.Environmental science and pollution research international · 2022Article
- A Preliminary Study of the Effect of Quercetin on Cytotoxicity, Apoptosis, and Stress Responses in Glioblastoma Cell Lines.International journal of molecular sciences · 2022Article
- Silica Nanoparticle Acute Toxicity on MaleFrontiers in bioengineering and biotechnology · 2022Article
- An Open Question: Is Non-Ionizing Radiation a Tool for Controlling Apoptosis-Induced Proliferation?International journal of molecular sciences · 2021Review
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionRecently, the focus of oncological research has been on the optimization of therapeutic strategies targeted at malignant diseases. Nanomedicine utilizing silicon dioxide nanoparticles (SiNPs) is one such strategy and is rapidly developing as a promising tool for cancer diagnosis, imaging, and treatment. Nevertheless, little is known about the mechanisms of action of SiNPs in brain tumors. MATERIALS AND
methodsHere, we explored the effects of 5-15 nm SiNPs in the human glioblastoma cell line LN229. In this respect, MTT assays, microscopic observations, flow cytometry analyses, and luminescent assays were performed. Moreover, RT-qPCR and Western blot analyses were done to determine gene and protein expressions.
resultsWe demonstrated that SiNPs triggered evident cytotoxicity, with microscopic observations of the nuclei, annexin V-fluorescein isothiocyanate/propidium iodide staining, and elevated caspase 3/7 activity, suggesting that SiNPs predominantly induced apoptotic death in LN229 cells. We further showed the occurrence of oxidative stress induced by enhanced reactive oxygen-species generation. This effect was followed by deregulated expression of genes encoding the antioxidant enzymes SOD1, SOD2, and CAT, and impaired mitochondria function. SiNP- induced mitochondrial dysfunction was characterized by membrane-potential collapse, ATP depletion, elevated expression of
conclusionsAltogether, our data indicate that in LN229 cells, SiNPs evoke cell death via activation of the intrinsic apoptosis pathway and suggest that other aspects of cellular function may also be affected. As such, SiNPs represent a potentially promising agent for facilitating further progress in brain cancer therapy. However, further exploration of SiNP long-term toxicity and molecular effects is necessary prior to their widespread application.
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