ArticleOncogene2019
Pathogenic mutations in neurofibromin identifies a leucine-rich domain regulating glioma cell invasiveness.
Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 29 citations in OpenAlex.
- NF1 Leucine Rich Domain-Derived Extracellular Vesicles Remodel the Glioblastoma Immune Microenvironment via an ADAM17-Associated Inflammatory Program.Journal of extracellular vesicles · 2026Article
- Single-cell and bulk transcriptome analysis reveals the impact of inflammatory microglia on prognosis and immunotherapy response in primary glioblastoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Review
- Zebrafish models in glioma research: advances in methodologies, mechanistic insights, and therapeutic frontiers.Frontiers in immunology · 2025Review
- Identifying Diffuse Glioma Subtypes Based on Pathway Enrichment Evaluation.Interdisciplinary sciences, computational life sciences · 2024Article
- [Gene therapy strategies and prospects for neurofibromatosis type 1].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2024Article
- Novel sights on therapeutic, prognostic, and diagnostics aspects of non-coding RNAs in glioblastoma multiforme.Metabolic brain disease · 2023Review
- Cellular and molecular features related to exceptional therapy response and extreme long-term survival in glioblastoma.Cancer medicine · 2023Review
- The therapeutic potential of neurofibromin signaling pathways and binding partners.Communications biology · 2023Review
- Functional Assays Combined with Pre-mRNA-Splicing Analysis Improve Variant Classification and Diagnostics for Individuals with Neurofibromatosis Type 1 and Legius Syndrome.Human mutation · 2023Article
- Review
- Gene Expression Profiling of Glioblastoma to Recognize Potential Biomarker Candidates.Frontiers in genetics · 2022Article
- Discovering Innate Driver Variants for Risk Assessment of Early Colorectal Cancer Metastasis.Frontiers in oncology · 2022Article
- Review
- Present and Future of Anti-Glioblastoma Therapies: A Deep Look into Molecular Dependencies/Features.Molecules (Basel, Switzerland) · 2020Review
- Molecular Heterogeneity and Immunosuppressive Microenvironment in Glioblastoma.Frontiers in immunology · 2020Review
- Potential biomarkers and challenges in glioma diagnosis, therapy and prognosis.BMJ neurology open · 2020Review
- Breast cancer risk (un)awareness among women suffering from neurofibromatosis type 1 in Poland.Contemporary oncology (Poznan, Poland) · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is the most aggressive tumor of the brain. NF1, a tumor suppressor gene and RAS-GTPase, is one of the highly mutated genes in GBM. Dysregulated NF1 expression promotes cell invasion, proliferation, and tumorigenesis. Loss of NF1 expression in glioblastoma is associated with increased aggressiveness of the tumor. Here, we show that NF1-loss in patient-derived glioma cells using shRNA increases self-renewal, heightens cell invasion, and promotes mesenchymal subtype and epithelial mesenchymal transition-specific gene expression that enhances tumorigenesis. The neurofibromin protein contains at least four major domains, with the GAP-related domain being the most well-studied. In this study, we report that the leucine-rich domain (LRD) of neurofibromin inhibits invasion of human glioblastoma cells without affecting their proliferation. Moreover, under conditions tested, the NF1-LRD fails to hydrolyze Ras-GTP to Ras-GDP, suggesting that its suppressive function is independent of Ras signaling. We further demonstrate that rare variants within the NF1-LRD domain found in a subset of the patients are pathogenic and reduce NF1-LRD's invasion suppressive function. Taken together, our results show, for the first time, that NF1-LRD inhibits glioma invasion, and provides evidence of a previously unrecognized function of NF1-LRD in glioma biology.
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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.