ArticleMolecular therapy. Nucleic acids2018
Effects of Aptamer to U87-EGFRvIII Cells on the Proliferation, Radiosensitivity, and Radiotherapy of Glioblastoma Cells.
Article in Molecular therapy. Nucleic acids, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 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.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 43 citations in OpenAlex.
- Molecular Engineering of Aptamers for Glioblastoma Therapy: From Simple Antagonists to AI-Driven Approaches, a Narrative Review.International journal of molecular sciences · 2026Review
- RNA-based precision medicine in glioblastoma driven by oncogenic gene fusions.Molecular therapy. Oncology · 2026Review
- Aptamer-functionalized exosomes combined with doxorubicin suppress GBM progression and enhance chemoradiosensitivity by promoting pyroptosis.Materials today. Bio · 2026Article
- New Player in the Field of Glioblastoma Therapy: EGFRvIII-Specific Gol1 Aptamer Shows a Great Therapeutic Potential.Pharmaceutics · 2026Article
- The Aptamer bi-(AID-1-T) Synergizes with Radiation to Inhibit Proliferation of Human Glioma Cells.Pharmaceutics · 2025Article
- In Silico Born Designed Anti-EGFR Aptamer Gol1 Has Anti-Proliferative Potential for Patient Glioblastoma Cells.International journal of molecular sciences · 2025Article
- A PET-CT study of the uptake of labeled aptamers [Frontiers in oncology · 2025Article
- Aptamers in Combination Therapies for Enhanced Radiosensitization in Cancer.Iranian journal of biotechnology · 2025Review
- Current landscape and future directions of targeted-alpha-therapy for glioblastoma treatment.Theranostics · 2025Review
- Aptamers as an approach to targeted cancer therapy.Cancer cell international · 2024Review
- Aptamers in neuro-oncology: An emerging therapeutic modality.Neuro-oncology · 2024Review
- Targeting lung cancer with clinically relevant EGFR mutations using anti-EGFR RNA aptamer.Molecular therapy. Nucleic acids · 2023Article
- Review
- A Novel and Highly Selective Epidermal Growth Factor Receptor Inhibitor, SMUZ106, for the Treatment of Glioblastoma.Pharmaceutics · 2023Article
- Radiochemical Synthesis of 4-[Molecules (Basel, Switzerland) · 2022Article
- Therapeutic Potential of Aptamer-Protein Interactions.ACS pharmacology & translational science · 2022Review
- The phosphatase of regenerating liver-3 protein (PRL-3) promotes glioma cell invasiveness by interacting with β3 -tubulin.Bioengineered · 2022Article
- Aptamer Applications in Neuroscience.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Novel Receptor Tyrosine Kinase Pathway Inhibitors for Targeted Radionuclide Therapy of Glioblastoma.Pharmaceuticals (Basel, Switzerland) · 2021Review
- A perspective on the radiopharmaceutical requirements for imaging and therapy of glioblastoma.Theranostics · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is the most prevalent and lethal malignant intracranial tumor in the brain, with very poor prognosis and survival. The epidermal growth factor receptor variant III (EGFRvIII) contributes to increased oncogenicity that does not occur through binding EGFR ligands and instead occurs through constitutive activation, which enhances glioma tumorigenicity and resistance to targeted therapy. Aptamers are nucleic acids with high affinity and specificity to targets selected by systematic evolution of ligands by exponential enrichment (SELEX), and are usually developed as antagonists of disease-associated factors. Herein, we generated a DNA aptamer U2, targeting U87-EGFRvIII cells, and demonstrated that U2 alters the U87-EGFRvIII cell growth, radiosensitivity, and radiotherapy of glioblastoma cells. We detected U2 and U87-EGFRvIII cells by flow cytometry and confocal microscopy to explore the binding ability of U2 to U87-EGFRvIII cells. Then, we found that aptamer U2 inhibits the proliferation, migration, invasion, and downstream signaling of U87-EGFRvIII cells. Moreover, the U2 aptamer can increase the radiosensitivity of U87-EGFRvIII in vitro and has a better antitumor effect on
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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.