ArticleThe Journal of clinical investigation2012
Attenuated adenosine-to-inosine editing of microRNA-376a* promotes invasiveness of glioblastoma cells.
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 135 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.
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Who cites it
135 citing papers in PubMed, 205 citations in OpenAlex.
- Review
- Evolution of Engineered ADAR-Based RNA Editing Systems.International journal of molecular sciences · 2026Review
- Adenosine-to-inosine editing of miR-200b-3p is associated with the progression of high-grade serous ovarian cancer.Molecular oncology · 2026Article
- Characterizing miRNA editing patterns in 5 types of cells using single-cell small RNA sequencing data.Frontiers in bioinformatics · 2026Article
- Targeting ADAR stability: a novel approach to combat glioblastoma.Frontiers in oncology · 2026Article
- Exosomal microRNAs: A new role in the diagnosis and treatment of lung cancer metastases (Review).International journal of oncology · 2025Review
- Rewriting the Fate of Cancer: Epigenetic and Epitranscriptomic Regulators in the Metastatic Cascade.Biomolecules · 2025Review
- Advances in RNA-based cancer therapeutics: pre-clinical and clinical implications.Molecular cancer · 2025Review
- miR-376a/Neuropilin-1 axis mediates the cancer stemness in oral squamous cell carcinoma-an in vitro study.Journal of dental sciences · 2025Article
- The Life of MicroRNAs: Biogenesis, Function and Decay in Cancer.Biomolecules · 2025Review
- Adenosine-to-inosine RNA editing in cancer: molecular mechanisms and downstream targets.Protein & cell · 2025Review
- The subventricular zone structure, function and implications for neurological disease.Genes & diseases · 2025Review
- Computer-Aided Discovery of Natural Compounds Targeting the ADAR2 dsRBD2-RNA Interface and Computational Modeling of Full-Length ADAR2 Protein Structure.International journal of molecular sciences · 2025Article
- Review
- ncRNA Editing: Functional Characterization and Computational Resources.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Identification of cancer driver genes based on hierarchical weak consensus model.Health information science and systems · 2024Article
- RNA-binding proteins and exoribonucleases modulating miRNA in cancer: the enemy within.Experimental & molecular medicine · 2024Review
- ADAR Family Proteins: A Structural Review.Current issues in molecular biology · 2024Review
- RNA modifications in cellular metabolism: implications for metabolism-targeted therapy and immunotherapy.Signal transduction and targeted therapy · 2024Review
- The role of ADAR1 through and beyond its editing activity in cancer.Cell communication and signaling : CCS · 2024Review
75 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the human brain, microRNAs (miRNAs) from the microRNA-376 (miR-376) cluster undergo programmed "seed" sequence modifications by adenosine-to-inosine (A-to-I) editing. Emerging evidence suggests a link between impaired A-to-I editing and cancer, particularly in high-grade gliomas. We hypothesized that disruption of A-to-I editing alters expression of genes regulating glioma tumor phenotypes. By sequencing the miR-376 cluster, we show that the overall miRNA editing frequencies were reduced in human gliomas. Specifically in high-grade gliomas, miR-376a* accumulated entirely in an unedited form. Clinically, a significant correlation was found between accumulation of unedited miR-376a* and the extent of invasive tumor spread as measured by magnetic resonance imaging of patient brains. Using both in vitro and orthotopic xenograft mouse models, we demonstrated that the unedited miR-376a* promoted glioma cell migration and invasion, while the edited miR-376a* suppressed these features. The effects of the unedited miR-376a* were mediated by its sequence-dependent ability to target RAP2A and concomitant inability to target AMFR. Thus, the tumor-dependent introduction of a single base difference in the miR-376a* sequence dramatically alters the selection of its target genes and redirects its function from inhibiting to promoting glioma cell invasion. These findings uncover a new mechanism of miRNA deregulation and identify unedited miR-376a* as a potential therapeutic target in glioblastoma cells.
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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.