ArticleScientific reports2018
Blocking distinct interactions between Glioblastoma cells and their tissue microenvironment: A novel multi-targeted therapeutic approach.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Interactions of ACEA and WIN 55,212-2 mesylate with temozolomide and cisplatin in neuroblastoma and glioblastoma cell lines: an isobolographic analysis.Pharmacological reports : PR · 2026Article
- De Novo Gene Transcription of Connexin Mediates Cytoplasmic Fluid Exchange and Flocking Transitions in Physiological and Cancerous Epithelial Systems.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Gap Junction Inhibitor Octanol Decreases Proliferation and Increases Glial Differentiation of Postnatal Neural Progenitor Cells.International journal of molecular sciences · 2024Article
- The Potential Role of the Extracellular Matrix Glycoprotein Reelin in Glioblastoma Biology.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Unraveling the intricate link between cell death and neuroinflammation usingFrontiers in cell and developmental biology · 2024Review
- Cellular Conversations in Glioblastoma Progression, Diagnosis and Treatment.Cellular and molecular neurobiology · 2023Review
- Article
- Disulfiram in glioma: Literature review of drug repurposing.Frontiers in pharmacology · 2022Review
- Repurposing Disulfiram for Targeting of Glioblastoma Stem Cells: An In Vitro Study.Biomolecules · 2021Article
- Molecular Mechanisms of Treatment Resistance in Glioblastoma.International journal of molecular sciences · 2020Review
- Collective invasion of glioma cells through OCT1 signalling and interaction with reactive astrocytes after surgery.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020Article
- The biological activity of bispecific trastuzumab/pertuzumab plant biosimilars may be drastically boosted by disulfiram increasing formaldehyde accumulation in cancer cells.Scientific reports · 2019Article
- Article
- Inflammation and Metabolism in Cancer Cell-Mitochondria Key Player.Frontiers in oncology · 2019Review
- Role of extracellular matrix and microenvironment in regulation of tumor growth and LAR-mediated invasion in glioblastoma.PloS one · 2018Article
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Due to the highly invasive nature of Glioblastoma (GB), complete surgical resection is not feasible, while motile tumour cells are often associated with several specific brain structures that enhance treatment-resistance. Here, we investigate the therapeutic potential of Disulfiram and Carbenoxolone, that inhibit two distinct interactions between GB and the brain tissue microenvironment: stress-induced cell-matrix adhesion and gap junction mediated cell-cell communication, respectively. Increase in cell numbers of tumour-initiating cells, which are cultured in suspension as cell clusters, and adherent differentiated cells can be blocked to a similar extent by Carbenoxolone, as both cell populations form gap junctions, but the adherent differentiated cells are much more sensitive to Disulfiram treatment, which - via modulation of NF-κB signalling - interferes with cell-substrate adhesion. Interestingly, inducing adhesion in tumour-initiating cells without differentiating them does not sensitize for Disulfiram. Importantly, combining Disulfiram, Carbenoxolone and the standard chemotherapeutic drug Temozolomide reduces tumour size in an orthotopic mouse model. Isolating GB cells from their direct environment within the brain represents an important addition to current therapeutic approaches. The blockage of cellular interactions via the clinically relevant substances Disulfiram and Carbenoxolone, has distinct effects on different cell populations within a tumour, potentially reducing motility and/or resistance to apoptosis.
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Registered trials
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