ArticleOncogenesis2020
Nuclear factor IX promotes glioblastoma development through transcriptional activation of Ezrin.
Article in Oncogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Tracing the origins of glioblastoma by investigating the role of gliogenic and related neurogenic genes/signaling pathways in GBM development: a systematic review.World journal of surgical oncology · 2022Pooled it
- Protein arginine methylation and ubiquitination: A prominent crosstalk and its functions in cancer.Genes & diseases · 2026Review
- An ALKBH3 Inhibitor HUHS199 Suppresses Proliferation of Glioblastoma Cells by Targeting 1-Methyladenosine on GADD45A mRNA.Chemical biology & drug design · 2026Article
- Downregulation of NFIA facilitates glycolysis, histone lactylation, and activation of the FN1-integrin α5β1 pathway in pancreatic cancer.Apoptosis : an international journal on programmed cell death · 2026Article
- NFIX suppresses breast cancer cell proliferation by delaying mitosis through downregulation of CDK1 expression.Cell death discovery · 2025Article
- mir-744-5p inhibits cell growth and angiogenesis in osteosarcoma by targeting NFIX.Journal of orthopaedic surgery and research · 2024Article
- ALOX5 contributes to glioma progression by promoting 5-HETE-mediated immunosuppressive M2 polarization and PD-L1 expression of glioma-associated microglia/macrophages.Journal for immunotherapy of cancer · 2024Article
- Gene regulatory network topology governs resistance and treatment escape in glioma stem-like cells.Science advances · 2024Article
- CREB5 promotes the proliferation and self-renewal ability of glioma stem cells.Cell death discovery · 2024Article
- Antioxidant network-based signatures cluster glioblastoma into distinct redox-resistant phenotypes.Frontiers in immunology · 2024Article
- Circular RNA hsa_circ_0049657 as a Potential Biomarker in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2023Article
- NFIXing Cancer: The Role of NFIX in Oxidative Stress Response and Cell Fate.International journal of molecular sciences · 2023Review
- Orphan nuclear receptor TLX promotes immunosuppression via its transcriptional activation of PD-L1 in glioma.Journal for immunotherapy of cancer · 2021Article
- miR-18a promotes glioblastoma development by down-regulating ALOXE3-mediated ferroptotic and anti-migration activities.Oncogenesis · 2021Article
- CircGLIS3 Promotes High-Grade Glioma Invasion via Modulating Ezrin Phosphorylation.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Enhanced migration is pivotal for the malignant development of glioblastoma (GBM), but the underlying molecular mechanism that modulates the migration of the GBM cells remains obscure. Here we show that nuclear factor IX (NFIX) is significantly upregulated in human GBM lesions compared with normal or low-grade gliomas. NFIX deficiency impairs the migration of GBM cells and inhibits the tumor growth in the hippocampus of immunodeficient nude mice. Mechanistically, NFIX silencing suppresses the expression of Ezrin, a protein that crosslinks actin cytoskeleton and plasma membrane, which is also positively correlated with GBM malignancy. NFIX depletion induced migration inhibition of GBM cells can be rescued by the replenishment of Ezrin. Furthermore, we identify a NFIX response element (RE) between -840 and -825 bp in the promoter region of the Ezrin gene. Altogether, our findings show, for the first time that NFIX can transcriptionally upregulate the expression of Ezrin and contribute to the enhanced migration of GBM cells, suggesting that NFIX is a potential target for GBM therapy.
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.