ArticlePloS one2013
miR-219-5p inhibits receptor tyrosine kinase pathway by targeting EGFR in glioblastoma.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- SALL4 and microRNA: The Role of Let-7.Genes · 2021Pooled it
- Overexpression of miR-219 as a potential therapeutic strategy of glioblastoma cells in vitro.Scientific reports · 2026Article
- MicroRNA-based integrated diagnosis and therapy for GBM: current status and advances.Frontiers in immunology · 2026Review
- Natural compounds as regulators of miRNAs: exploring a new avenue for treating brain cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Novel strategy to target glioblastoma-initiating cells using a braintropic adeno-associated virus carrying a miR-dependent genome-editing system.British journal of cancer · 2025Article
- The role of lncRNAs in the interplay of signaling pathways and epigenetic mechanisms in glioma.Epigenomics · 2025Review
- MicroRNA-219 in the central nervous system: a potential theranostic approach.Research in pharmaceutical sciences · 2024Review
- Practical immunomodulatory landscape of glioblastoma multiforme (GBM) therapy.Journal of the Egyptian National Cancer Institute · 2024Review
- An Overview of EGFR Mechanisms and Their Implications in Targeted Therapies for Glioblastoma.International journal of molecular sciences · 2023Review
- Crosstalk of Epigenetic and Metabolic Signaling Underpinning Glioblastoma Pathogenesis.Cancers · 2022Review
- Functions of non-coding RNAs in regulating cancer drug targets.Acta biochimica et biophysica Sinica · 2022Review
- Selective sodium iodide symporter (Molecular therapy oncolytics · 2021Article
- mTOR-Rictor-EGFR axis in oncogenesis and diagnosis of glioblastoma multiforme.Molecular biology reports · 2021Review
- MicroRNA 219-5p inhibits alveolarization by reducing platelet derived growth factor receptor-alpha.Respiratory research · 2021Article
- miR-219a-1 inhibits colon cancer cells proliferation and invasion by targetingCancer biology & therapy · 2020Article
- Critical role of HOX transcript antisense intergenic RNA (HOTAIR) in gliomas.Journal of molecular medicine (Berlin, Germany) · 2020Review
- The Roles of miRNA in Glioblastoma Tumor Cell Communication: Diplomatic and Aggressive Negotiations.International journal of molecular sciences · 2020Review
- microRNA-219-5p targets NEK6 to inhibit hepatocellular carcinoma progression.American journal of translational research · 2020Article
- miR-557 inhibits the proliferation and invasion of pancreatic cancer cells by targeting EGFR.International journal of clinical and experimental pathology · 2019Article
- MicroRNAs in Microglia: How do MicroRNAs Affect Activation, Inflammation, Polarization of Microglia and Mediate the Interaction Between Microglia and Glioma?Frontiers in molecular neuroscience · 2019Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma is one of the common types of primary brain tumors with a median survival of 12-15 months. The receptor tyrosine kinase (RTK) pathway is known to be deregulated in 88% of the patients with glioblastoma. 45% of GBM patients show amplifications and activating mutations in EGFR gene leading to the upregulation of the pathway. In the present study, we demonstrate that a brain specific miRNA, miR-219-5p, repressed EGFR by directly binding to its 3'-UTR. The expression of miR-219-5p was downregulated in glioblastoma and the overexpression of miR-219-5p in glioma cell lines inhibited the proliferation, anchorage independent growth and migration. In addition, miR-219-5p inhibited MAPK and PI3K pathways in glioma cell lines in concordance with its ability to target EGFR. The inhibitory effect of miR-219-5p on MAPK and PI3K pathways and glioma cell migration could be rescued by the overexpression of wild type EGFR and vIII mutant of EGFR (both lacking 3'-UTR and thus being insensitive to miR-219-5p) suggesting that the inhibitory effects of miR-219-5p were indeed because of its ability to target EGFR. We also found significant negative correlation between miR-219-5p levels and total as well as phosphorylated forms of EGFR in glioblastoma patient samples. This indicated that the downregulation of miR-219-5p in glioblastoma patients contribute to the increased activity of the RTK pathway by the upregulation of EGFR. Thus, we have identified and characterized miR-219-5p as the RTK regulating novel tumor suppressor miRNA in glioblastoma.
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