ArticleBrain : a journal of neurology2021
Stepwise crosstalk between aberrant Nf1, Tp53 and Rb signalling pathways induces gliomagenesis in zebrafish.
Article in Brain : a journal of neurology, 2021. 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, 17 citations in OpenAlex.
- Mutation of Tubgcp6 induces hematopoietic stem and progenitor cell exhaustion in zebrafish.Communications biology · 2026Article
- Review
- ITPKA suppresses glioma progression and predicts patient prognosis.Frontiers in oncology · 2026Article
- Par6/SOX2 interact to modulate stemness maintenance in glioma by regulating the EGFR/PI3K/AKT signaling cascade.Oncogene · 2025Article
- Telomeres, telomerase, and cancer: mechanisms, biomarkers, and therapeutics.Experimental hematology & oncology · 2025Review
- Nitric oxide-primed engineered extracellular vesicles restore bioenergetics in acute kidney injury via mitochondrial transfer.Theranostics · 2025Article
- Zebrafish models in glioma research: advances in methodologies, mechanistic insights, and therapeutic frontiers.Frontiers in immunology · 2025Review
- A case report on IDH-mutant astrocytoma, CNS WHO grade 4: multi-omic characterization of untreated clinical progression.Frontiers in oncology · 2025Article
- Unraveling neuronal and metabolic alterations in neurofibromatosis type 1.Journal of neurodevelopmental disorders · 2024Review
- Role of RB1 in neurodegenerative diseases: inhibition of post-mitotic neuronal apoptosis via Kmt5b.Cell death discovery · 2024Article
- Intra-Operative Definition of Glioma Infiltrative Margins by Visualizing Immunosuppressive Tumor-Associated Macrophages.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Sulindac selectively induces autophagic apoptosis of GABAergic neurons and alters motor behaviour in zebrafish.Nature communications · 2023Article
- Loss of p53 Concurrent with RAS and TERT Activation Induces Glioma Formation.Molecular neurobiology · 2023Article
- Pediatric low-grade glioma models: advances and ongoing challenges.Frontiers in oncology · 2023Review
- Prognostic features and comprehensive genomic analysis of NF1 mutations in EGFR mutant lung cancer patients.Cancer medicine · 2023Article
- Current understanding of gliomagenesis: from model to mechanism.International journal of medical sciences · 2022Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular pathogenesis of glioblastoma indicates that RTK/Ras/PI3K, RB and TP53 pathways are critical for human gliomagenesis. Here, several transgenic zebrafish lines with single or multiple deletions of nf1, tp53 and rb1 in astrocytes, were established to genetically induce gliomagenesis in zebrafish. In the mutant with a single deletion, we found only the nf1 mutation low-efficiently induced tumour incidence, suggesting that the Nf1 pathway is critical for the initiation of gliomagenesis in zebrafish. Combination of mutations, nf1;tp53 and rb1;tp53 combined knockout fish, showed much higher tumour incidences, high-grade histology, increased invasiveness, and shortened survival time. Further bioinformatics analyses demonstrated the alterations in RTK/Ras/PI3K, cell cycle, and focal adhesion pathways, induced by abrogated nf1, tp53, or rb1, were probably the critical stepwise biological events for the initiation and development of gliomagenesis in zebrafish. Gene expression profiling and histological analyses showed the tumours derived from zebrafish have significant similarities to the subgroups of human gliomas. Furthermore, temozolomide treatment effectively suppressed gliomagenesis in these glioma zebrafish models, and the histological responses in temozolomide-treated zebrafish were similar to those observed in clinically treated glioma patients. Thus, our findings will offer a potential tool for genetically investigating gliomagenesis and screening potential targeted anti-tumour compounds for glioma treatment.
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