ArticleThe Journal of clinical investigation2012
TGF-β induces miR-182 to sustain NF-κB activation in glioma subsets.
Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers.
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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
128 citing papers in PubMed, 215 citations in OpenAlex.
- CRYM suppresses glioblastoma progression by inhibiting the TGFβ1/Smad-EMT signaling pathway.Journal of neuro-oncology · 2026Article
- The deubiquitinase OTUD1 orchestrates cisplatin chemosensitivity of non-small cell lung cancer through destabilizing RAD23B/XPC.Oncogene · 2025Article
- Targeting TGF-β signaling in glioblastoma: therapeutic implications and novel drug development strategies.Brain tumor pathology · 2025Review
- The Pivotal Role of NF-κB in Glioblastoma: Mechanisms of Activation and Therapeutic Implications.International journal of molecular sciences · 2025Review
- Decoding NF-κB: nucleocytoplasmic shuttling dynamics, synthetic modulation and post-therapeutic behavior in cancer.Molecular biology reports · 2025Review
- Role of CYLD in brain physiology and pathology.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Unmasking the potential: mechanisms of neuroinflammatory modulation by oncolytic viruses in glioblastoma.Exploration of targeted anti-tumor therapy · 2025Review
- Bioinformatics Study and Experimental Evaluation of miR-182, and miR-34 Expression Profiles in Tuberculosis and Lung Cancer.Tuberculosis and respiratory diseases · 2024Article
- PL-hMSC and CH-hMSC derived soluble factors inhibit proliferation but improve hGBM cell migration by activating TGF-β and inhibiting Wnt signaling.Bioscience reports · 2024Article
- IDH1 mutation produces R-2-hydroxyglutarate (R-2HG) and induces mir-182-5p expression to regulate cell cycle and tumor formation in glioma.Biological research · 2024Article
- NF-κB in biology and targeted therapy: new insights and translational implications.Signal transduction and targeted therapy · 2024Review
- Use of microRNAs as Diagnostic, Prognostic, and Therapeutic Tools for Glioblastoma.International journal of molecular sciences · 2024Review
- SECTM1 promotes the development of glioblastoma and mesenchymal transition by regulating the TGFβ1/Smad signaling pathway.International journal of biological sciences · 2024Article
- CD109, a master regulator of inflammatory responses.Frontiers in immunology · 2024Review
- Review
- Essential role of the amino-terminal region of Drosha for the Microprocessor function.iScience · 2023Article
- Role of Non-Coding RNAs in TGF-β Signalling in Glioma.Brain sciences · 2023Review
- MiR-182-5p Is Upregulated in Hepatic Tissues from a Diet-Induced NAFLD/NASH/HCC C57BL/6J Mouse Model and Modulates Cyld and Foxo1 Expression.International journal of molecular sciences · 2023Article
- SPATA2 suppresses epithelial-mesenchymal transition to inhibit metastasis and radiotherapy sensitivity in non-small cell lung cancer via impairing DVL1/β-catenin signaling.Thoracic cancer · 2023Article
- Differential Transcriptome Responses in Human THP-1 Macrophages Following Exposure to T98G and LN-18 Human Glioblastoma Secretions: A Simplified Bioinformatics Approach to Understanding Patient-Glioma-Specific Effects on Tumor-Associated Macrophages.International journal of molecular sciences · 2023Article
68 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
The strength and duration of NF-κB signaling are tightly controlled by multiple negative feedback mechanisms. However, in cancer cells, these feedback loops are overridden through unclear mechanisms to sustain oncogenic activation of NF-κB signaling. Previously, we demonstrated that overexpression of miR-30e* directly represses IκBα expression and leads to hyperactivation of NF-κB. Here, we report that miR-182 was overexpressed in a different set of gliomas with relatively lower miR-30e* expression and that miR-182 directly suppressed cylindromatosis (CYLD), an NF-κB negative regulator. This suppression of CYLD promoted ubiquitin conjugation of NF-κB signaling pathway components and induction of an aggressive phenotype of glioma cells both in vitro and in vivo. Furthermore, we found that TGF-β induced miR-182 expression, leading to prolonged NF-κB activation. Importantly, the results of these experiments were consistent with an identified significant correlation between miR-182 levels with TGF-β hyperactivation and activated NF-κB in a cohort of human glioma specimens. These findings uncover a plausible mechanism for sustained NF-κB activation in malignant gliomas and may suggest a new target for clinical intervention in human cancer.
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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.