ArticleFrontiers in oncology2021
Cyclovirobuxine D Induces Apoptosis and Mitochondrial Damage in Glioblastoma Cells Through ROS-Mediated Mitochondrial Translocation of Cofilin.
Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- TEAD4-driven GPX8 promotes temozolomide resistance in glioma by facilitating CTHRC1 expression to suppress mitochondrial oxidative stress.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- A Novel Pyrazole Pyrimidine Derivative MBP346 Induces Cell Death via ROS-Mediated Mitochondrial Damage in Human Head and Neck Squamous Cell Carcinoma.Molecules (Basel, Switzerland) · 2026Article
- Cyclovirobuxine D attenuates collagen-induced arthritis by inhibiting PI3K/AKT pathway and macrophage polarization.Arthritis research & therapy · 2026Article
- Cyclovirobuxine D suppresses cancer stemness in osteosarcoma with implication of the noncanonical NF-kappaB pathway.Frontiers in pharmacology · 2026Article
- Cyclovirobuxine D ameliorates cardiomyocyte senescence in diabetic cardiomyopathy mice by enhancing mitochondrial function via sirtuin 3-ATP5O signal axis.Chinese medicine · 2025Article
- Article
- Plant Alkaloids as Promising Anticancer Compounds with Blood-Brain Barrier Penetration in the Treatment of Glioblastoma: In Vitro and In Vivo Models.Molecules (Basel, Switzerland) · 2025Review
- Versatile Nanomaterials That Interfere with Ferroptosis in the Tumor Microenvironment.International journal of nanomedicine · 2025Review
- Ultrastructural Changes of Neuroendocrine Pheochromocytoma Cell Line PC-12 Exposed In Vitro to Rotenone.Brain sciences · 2024Article
- DNA repair pathways-targeted cyclovirobuxine inhibits castration-resistant prostate cancer growth by promoting cell apoptosis and cycle arrest.Translational oncology · 2023Article
- Calycosin as a Novel PI3K Activator Reduces Inflammation and Fibrosis in Heart Failure Through AKT-IKK/STAT3 Axis.Frontiers in pharmacology · 2022Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCyclovirobuxine D (CVBD), a steroidal alkaloid, has multiple pharmacological activities, including anti-cancer activity. However, the anti-cancer effect of CVBD on glioblastoma (GBM) has seldom been investigated. This study explores the activity of CVBD in inducing apoptosis of GBM cells, and examines the related mechanism in depth.
methodsGBM cell lines (T98G, U251) and normal human astrocytes (HA) were treated with CVBD. Cell viability was examined by CCK-8 assay, and cell proliferation was evaluated by cell colony formation counts. Apoptosis and mitochondrial superoxide were measured by flow cytometry. All protein expression levels were determined by Western blotting. JC-1 and CM-H
resultsCVBD showed a greater anti-proliferation effect on the GBM cell lines, T98G and U251, than normal human astrocytes in dose- and time-dependent manners. CVBD induced apoptosis and mitochondrial damage in GBM cells. We found that CVBD led to mitochondrial translocation of cofilin. Knockdown of cofilin attenuated CVBD-induced apoptosis and mitochondrial damage. Additionally, the generation of ROS and mitochondrial superoxide was also induced by CVBD in a dose-dependent manner. N-acetyl-L-cysteine (NAC) and mitoquinone (MitoQ) pre-treatment reverted CVBD-induced apoptosis and mitochondrial damage. MitoQ pretreatment was able to block the mitochondrial translocation of cofilin caused by CVBD.
conclusionsOur data revealed that CVBD induced apoptosis and mitochondrial damage in GBM cells. The underlying mechanism is related to mitochondrial translocation of cofilin caused by mitochondrial oxidant stress.
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