ArticleNature neuroscience2015
Mitochondrial control by DRP1 in brain tumor initiating cells.
Article in Nature neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 263 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
263 citing papers in PubMed, 1 synthesis or guideline pooled it, 416 citations in OpenAlex.
- The Interplay of Microtubules with Mitochondria-ER Contact Sites (MERCs) in Glioblastoma.Biomolecules · 2022Pooled it
- Reactivation of DRP1 plays a functional role in resistance to MEK inhibition in pancreatic cancer cells.British journal of cancer · 2026Article
- Enhanced mitochondrial fission promotes chemosensitivity via SHP-1 activity in triple-negative breast cancer.Molecular biology reports · 2026Article
- Translational insights and clinical challenges of targeting cancer stem cells.Signal transduction and targeted therapy · 2026Review
- Fatty Acid Metabolism Rewires Glioblastoma Progression and Treg-Mediated Immune Resistance.Cancers · 2026Review
- From Ferroptotic Stress to Stemness: TNT-Mediated EMT Plasticity in Cancer Progression.Stem cell reviews and reports · 2026Review
- DRP1 and MID49 co-diffusion scans mitochondria for fission.Nature cell biology · 2026Article
- Reactivation of DRP1 plays a functional role in resistance to MEK inhibition in pancreatic cancer cells.bioRxiv : the preprint server for biology · 2026Article
- Newcastle disease virus hijacks mitophagy to reprogram amino acid metabolism for enhanced replication.Autophagy · 2026Article
- A Recombinant Antibody Against Human DRP1 Serine 616 Phosphorylation Enables Detection of BRAFAntibodies (Basel, Switzerland) · 2026Article
- Mitochondrial dynamics and cancer: mechanisms and targeted therapy.Cell biology and toxicology · 2026Review
- The evolving landscape of brain metastasis: volume II.Trends in cancer · 2026Review
- Mitochondrial retrograde signaling in gastric cancer: mtDNA mutations, ROS-driven NF-κB/HIF-1α activation, and Warburg effect amplification.Frontiers in physiology · 2026Review
- Mitochondrial metabolism in cancer stem cells (CSCs): molecular and diagnostic implications.Frontiers in molecular biosciences · 2026Review
- PPA2 activates MTFP1-DNM1L fission signaling to govern mitochondrial proliferation and mitophagy.Autophagy · 2026Article
- Multiple Mechanisms and Therapeutic Strategies for the Involvement of AMPK in the Development of Alzheimer's Disease.Molecular neurobiology · 2025Review
- Conformational Rearrangement of Fission DSPs.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Lactylation-driven USP4-mediated ANXA2 stabilization and activation promotes maintenance and radioresistance of glioblastoma stem cells.Cell death and differentiation · 2025Article
- Metabolic adaptations of brain metastasis.Nature reviews. Cancer · 2025Review
- Hypoxia inducible factor 1α-driven steroidogenesis impacts systemic hematopoiesis.Cellular & molecular biology letters · 2025Article
203 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
Brain tumor initiating cells (BTICs) co-opt the neuronal high affinity glucose transporter, GLUT3, to withstand metabolic stress. We investigated another mechanism critical to brain metabolism, mitochondrial morphology, in BTICs. BTIC mitochondria were fragmented relative to non-BTIC tumor cell mitochondria, suggesting that BTICs increase mitochondrial fission. The essential mediator of mitochondrial fission, dynamin-related protein 1 (DRP1), showed activating phosphorylation in BTICs and inhibitory phosphorylation in non-BTIC tumor cells. Targeting DRP1 using RNA interference or pharmacologic inhibition induced BTIC apoptosis and inhibited tumor growth. Downstream, DRP1 activity regulated the essential metabolic stress sensor, AMP-activated protein kinase (AMPK), and targeting AMPK rescued the effects of DRP1 disruption. Cyclin-dependent kinase 5 (CDK5) phosphorylated DRP1 to increase its activity in BTICs, whereas Ca(2+)-calmodulin-dependent protein kinase 2 (CAMK2) inhibited DRP1 in non-BTIC tumor cells, suggesting that tumor cell differentiation induces a regulatory switch in mitochondrial morphology. DRP1 activation correlated with poor prognosis in glioblastoma, suggesting that mitochondrial dynamics may represent a therapeutic target for BTICs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.