ArticleInternational journal of medical sciences2020
Mitochondrial dysfunction contributes to Rapamycin-induced apoptosis of Human Glioblastoma Cells - A synergistic effect with Temozolomide.
Article in International journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- Targeting metabolic mechanisms to overcome temozolomide resistance in glioblastoma.Discover oncology · 2026Review
- mTOR signaling networks: mechanistic insights and translational frontiers in disease therapeutics.Signal transduction and targeted therapy · 2025Review
- Autophagy-Related Proteins Influence Mouse Epididymal Sperm Motility.International journal of molecular sciences · 2025Article
- Non-immune targeting of CXCR3 compromises mitochondrial function and suppresses tumor growth in glioblastoma.Cell death discovery · 2025Article
- Mitochondrial micro RNAs: Crucial players in carcinogenesis.Oncology research · 2025Review
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- DRP1: At the Crossroads of Dysregulated Mitochondrial Dynamics and Altered Cell Signaling in Cancer Cells.ACS omega · 2023Review
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- Complex Interplay between Autophagy and Oxidative Stress in the Development of Endometriosis.Antioxidants (Basel, Switzerland) · 2022Article
- Response of Skin-Derived and Metastatic Human Malignant Melanoma Cell Lines to Thymoquinone and Thymoquinone-Loaded Liposomes.Pharmaceutics · 2022Article
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- Diaph3 underlines tumor cell heterogeneity in glioblastoma with implications for treatment modalities resistance.Journal of neuro-oncology · 2022Article
- Therapeutic strategies of glioblastoma (GBM): The current advances in the molecular targets and bioactive small molecule compounds.Acta pharmaceutica Sinica. B · 2022Review
- Oxidative Stress Activated by Sorafenib Alters the Temozolomide Sensitivity of Human Glioma Cells Through Autophagy and JAK2/STAT3-AIF Axis.Frontiers in cell and developmental biology · 2021Article
- Reaching the point-of-no-return: The cornerstone of glioblastoma treatment?Neuro-oncology advancesReview
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mammalian target of rapamycin (mTOR) is upregulated in a high percentage of glioblastomas. While a well-known mTOR inhibitor, rapamycin, has been shown to reduce glioblastoma survival, the role of mitochondria in achieving this therapeutic effect is less well known. Here, we examined mitochondrial dysfunction mechanisms that occur with the suppression of mTOR signaling. We found that, along with increased apoptosis, and a reduction in transformative potential, rapamycin treatment significantly affected mitochondrial health. Specifically, increased production of reactive oxygen species (ROS), depolarization of the mitochondrial membrane potential (MMP), and altered mitochondrial dynamics were observed. Furthermore, we verified the therapeutic potential of rapamycin-induced mitochondrial dysfunction through co-treatment with temzolomide (TMZ), the current standard of care for glioblastoma. Together these results demonstrate that the mitochondria remain a promising target for therapeutic intervention against human glioblastoma and that TMZ and rapamycin have a synergistic effect in suppressing glioblastoma viability, enhancing ROS production, and depolarizing MMP.
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Registered trials
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