ArticleJournal of cellular and molecular medicine2022
Interfering with mitochondrial dynamics sensitizes glioblastoma multiforme to temozolomide chemotherapy.
Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Redox Regulation in Glioblastoma: Mechanisms, Biomarkers, and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Specific targeting of cancer cell mitochondria with a malaria drug improves pancreatic cancer outcome.Scientific reports · 2026Article
- Imbalances of mitochondrial dynamics in solid tumors.Oncogenesis · 2026Review
- Mitochondrial DNA Content Modulates Chemosensitivity and Cellular Adaptation in Glioblastoma Cells.The Eurasian journal of medicine · 2026Article
- Revealing the Roles of the SH3GLB1-Hydrogen Peroxide Axis in Glioblastoma Multiforme Cells.Oncology research · 2026Article
- Severe Chemoradiotherapy Toxicity in a Pediatric Patient with Leigh Syndrome and Grade IV Isocitrate Dehydrogenase-Mutant Astrocytoma: A Case Report.The American journal of case reports · 2025Article
- Current status of traditional Chinese medicine in modulating mitochondrial metabolic abnormalities in tumors.Cancer biology & medicine · 2025Review
- DRP1, fission and apoptosis.Cell death discovery · 2025Review
- Article
- VEGFR2 blockade inhibits glioblastoma cell proliferation by enhancing mitochondrial biogenesis.Journal of translational medicine · 2024Article
- Targeting mitochondrial dynamics by AZD5363 in triple-negative breast cancer MDA-MB-231 cell-derived spheres.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- Multi-Omics Analyses Reveal Mitochondrial Dysfunction Contributing to Temozolomide Resistance in Glioblastoma Cells.Biomolecules · 2023Article
- Mitochondrial metabolism: a predictive biomarker of radiotherapy efficacy and toxicity.Journal of cancer research and clinical oncology · 2023Review
- Measurement of Patient-Derived Glioblastoma Cell Response to Temozolomide Using Fluorescence Lifetime Imaging of NAD(P)H.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Glioblastoma Metabolism: Insights and Therapeutic Strategies.International journal of molecular sciences · 2023Review
- Novel DZ-SIM Conjugate Targets Cancer Mitochondria and Prolongs Survival in Pancreatic Ductal Adenocarcinoma.Advanced therapeutics · 2022Article
- Interfering with mitochondrial dynamics sensitizes glioblastoma multiforme to temozolomide chemotherapy.Journal of cellular and molecular medicine · 2022Article
Corrections and comments
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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
Glioblastoma multiforme (GBM) is a primary tumour of the central nervous system (CNS) that exhibits the highest degree of malignancy. Radiotherapy and chemotherapy are essential to prolong the survival time of patients. However, clinical work has demonstrated that sensitivity of GBM to chemotherapy decreases with time. The phenomenon of multi-drug resistance (MDR) reminds us that there may exist some fundamental mechanisms in the process of chemo-resistance. We tried to explore the mechanism of GBM chemo-resistance from the perspective of energy metabolism. First, we found that the oxidative phosphorylation (OXPHOS) level of SHG44 and U87 cells increased under TMZ treatment. In further studies, it was found that the expression of PINK1 and mitophagy flux downstream was downregulated in GBM cells, which were secondary to the upregulation of TP53 in tumour cells under TMZ treatment. At the same time, we examined the mitochondrial morphology in tumour cells and found that the size of mitochondria in tumour cells increased under the treatment of TMZ, which originated from the regulation of AMPK on the subcellular localization of Drp1 under the condition of unbalanced energy supply and demand in tumour cells. The accumulation of mitochondrial mass and the optimization of mitochondrial quality accounted for the increased oxidative phosphorylation, and interruption of the mitochondrial fusion process downregulated the efficiency of oxidative phosphorylation and sensitized GBM cells to TMZ, which was also confirmed in the in vivo experiment. What is more, interfering with this process is an innovative strategy to overcome the chemo-resistance of GBM cells.
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