ArticleScientific reports2019
Suppression of glioblastoma by a drug cocktail reprogramming tumor cells into neuronal like cells.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
21 citing papers in PubMed.
- Neurogenic Small Molecules Reverse miR-342-3p-Mediated Tumorigenesis in Renal Cell Carcinoma.World journal of oncology · 2026Article
- Ferroptosis modulation enhances astrocyte-to-neuron conversion induced by a novel chemical cocktail in the hemorrhagic brain.Signal transduction and targeted therapy · 2026Article
- NeuroD1 gene therapy inhibits glioma growth and extends life span throughMolecular therapy. Oncology · 2026Article
- Cellular reprogramming of H3K27M pediatric high-grade glioma to neuron-like state.Acta neuropathologica communications · 2025Article
- Neuronal differentiation regulator CEND1 coordinately suppresses tumor growth and energetics via AMPK signaling in brain glioma.Cell & bioscience · 2025Article
- The tumor-associated fibrotic reactions in microenvironment aggravate glioma chemoresistance.Frontiers in oncology · 2024Review
- Regulation of Cell Plasticity by Bromodomain and Extraterminal Domain (BET) Proteins: A New Perspective in Glioblastoma Therapy.International journal of molecular sciences · 2023Review
- Dissecting cell fate dynamics in pediatric glioblastoma through the lens of complex systems and cellular cybernetics.Biological cybernetics · 2022Review
- Review
- Anti-glioblastoma effects of phenolic variants of benzoylphenoxyacetamide (BPA) with high potential for blood brain barrier penetration.Scientific reports · 2022Article
- Transcriptomic analysis reveals that coxsackievirus B3 Woodruff and GD strains use similar key genes to induce FoxO signaling pathway activation in HeLa cells.Archives of virology · 2022Article
- Application of Small Molecules in the Central Nervous System Direct Neuronal Reprogramming.Frontiers in bioengineering and biotechnology · 2022Review
- A Review of Mathematical and Computational Methods in Cancer Dynamics.Frontiers in oncology · 2022Review
- Rho-Kinase as a Target for Cancer Therapy and Its Immunotherapeutic Potential.International journal of molecular sciences · 2021Review
- SOCS3 is Related to Cell Proliferation in Neuronal Tissue: An Integrated Analysis of Bioinformatics and Experiments.Frontiers in genetics · 2021Article
- NF-κB inhibitor with Temozolomide results in significant apoptosis in glioblastoma via the NF-κB(p65) and actin cytoskeleton regulatory pathways.Scientific reports · 2020Article
- Imaging-AMARETTO: An Imaging Genomics Software Tool to Interrogate Multiomics Networks for Relevance to Radiography and Histopathology Imaging Biomarkers of Clinical Outcomes.JCO clinical cancer informatics · 2020Article
- To Become or Not to Become Tumorigenic: Subventricular ZoneFrontiers in oncology · 2020Review
- Prospects of Directly Reprogrammed Adult Human Neurons for Neurodegenerative Disease Modeling and Drug Discovery: iN vs. iPSCs Models.Frontiers in neuroscience · 2020Review
- Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is the most common and aggressive malignant tumor in adult brain. Even with the current standard therapy including surgical resection followed by postoperative radiotherapy and chemotherapy with temozolomide (Temo), GBM patients still have a poor median survival. Reprogramming of tumor cells into non-malignant cells might be a promising therapeutic strategy for malignant tumors, including GBM. Based on previous studies using small molecules to reprogram astrocytes into neuronal cells, here we further identified a FTT cocktail of three commonly used drugs (Fasudil, Tranilast, and Temo) to reprogram patient-derived GBM cells, either cultured in serum containing or serum-free medium, into neuronal like cells. FTT-treated GBM cells displayed a neuronal like morphology, expressed neuronal genes, exhibited neuronal electrophysiological properties, and showed attenuated malignancy. More importantly, FTT cocktail more significantly suppressed tumor growth and prolonged survival in GBM patient derived xenograft than Temo alone. Our study provided preclinical evidence that the neuronal reprogramming drug cocktail might be a promising strategy to improve the existing treatment for GBM.
Identifiers
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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.