ArticleOncogene2017
Tumour exosomes from cells harbouring PTPRZ1-MET fusion contribute to a malignant phenotype and temozolomide chemoresistance in glioblastoma.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 1 of them a synthesis that pooled it.
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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
87 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Research trends and hotspots in prostate cancer associated exosome: a bibliometric analysis.Frontiers in oncology · 2023Pooled it
- Vebreltinib for Previously Treated Astrocytoma,Cancer communications (London, England) · 2026Trial
- Clinicopathological Implications of IDH1 Mutation and Ki-67 Expression Across WHO Grades of Gliomas: Insights from a Prospective Observational Study.Iranian journal of pathology · 2026Article
- Spatial enrichment of PTPRZ1 in the peritumoral niche drives glioblastoma migration via the OPA1/ROS/CDH2 axis.Journal of translational medicine · 2026Article
- MET fusions and splicing variants in glioma: a landscape integrating clinical, pathological, and survival features.The journal of pathology. Clinical research · 2026Article
- Exosome crown proteins are promising markers for liquid biopsy of breast cancer.Frontiers in oncology · 2026Review
- The Role of Exosomal Biomarkers in the Monitoring of Bioactivation and Metabolite Clearance of Chemotherapeutics in Cancer Patients.Current drug metabolism · 2026Review
- Increased expression of FBW7 may improve the prognosis of lung adenocarcinoma after pemetrexed chemotherapy by transforming the epithelial-to-mesenchymal process.Journal of thoracic disease · 2025Article
- Exosomes in the Chemoresistance of Glioma: Key Point in Chemoresistance.Journal of cellular and molecular medicine · 2025Review
- NCAPH as a potential prognostic signaling biomarker regulating low-grade glioma cell proliferation, migration, invasion, immune microenvironment, and drug sensitivity.Journal of Cancer · 2025Article
- Glioblastoma stem cells deliver ABCB4 transcribed by ATF3 via exosomes conferring glioblastoma resistance to temozolomide.Cell death & disease · 2024Article
- AberrantCells · 2024Review
- MET alterations detection platforms and clinical implications in solid tumors: a comprehensive review of literature.Therapeutic advances in medical oncology · 2024Review
- Case report: GermlineFrontiers in oncology · 2024Article
- CBX2 enhances the progression and TMZ chemoresistance of glioma via EZH2-mediated epigenetic silencing of PTEN expression.Frontiers in pharmacology · 2024Article
- Patient-derived exosomes facilitate therapeutic targeting of oncogenic MET in advanced gastric cancer.Science advances · 2023Article
- Engineering a tunable micropattern-array assay to sort single extracellular vesicles and particles to detect RNA and protein in situ.Journal of extracellular vesicles · 2023Article
- PTPRZ1-METFUsion GENe (ZM-FUGEN) trial: study protocol for a multicentric, randomized, open-label phase II/III trial.Chinese neurosurgical journal · 2023Article
- Protein Tyrosine Phosphatase Receptor Zeta 1 as a Potential Target in Cancer Therapy and Diagnosis.International journal of molecular sciences · 2023Review
- Molecular Pathways Implicated in Radioresistance of Glioblastoma Multiforme: What Is the Role of Extracellular Vesicles?International journal of molecular sciences · 2023Review
27 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exosomes are carriers of pro-tumorigenic factors that participate in glioblastoma (GBM) progression, and many fusion genes are strong driver mutations in neoplasia and are involved in tumorigenesis. However, the ability of fusion genes to be transduced by exosomes is unknown. We characterized exosomes from GBM cells harbouring and not harbouring PTPRZ1-MET fusion (ZM fusion). We also determined the effect of the exosomes from ZM fusion cells (ZM exosomes) on pro-oncogenic secretions and showed that ZM exosomes are internalized by the recipient cells. In addition, we studied the effect of ZM exosome-mediated intercellular communication in the GBM microenvironment. MET proto-oncogene expression was higher in ZM exosomes. Moreover, phosphorylated MET was detected only in ZM exosomes and not in exosomes released by non-ZM fusion GBM cells. ZM exosomes transferred to non-ZM fusion GBM cells and normal human astrocytes altered gene expression and induced epithelial-mesenchymal transition. The uptake of ZM exosomes also induced an exosome-dependent phenotype defined by GBM cell migration and invasion, neurosphere growth and angiogenesis. In addition, ZM exosomes conferred temozolomide resistance to the GBM cells, and exosome-derived ZM fusion network proteins targeted multiple pro-oncogenic effectors in recipient cells within the GBM microenvironment. Our findings show that exosomes mediate the aggressive character of GBM and demonstrate the role of ZM fusion in the exacerbation of this effect. These findings have possible implications for the foundation of gene fusion-based therapy for managing GBM.
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