ArticleOncotarget2015
Aptamer targeting EGFRvIII mutant hampers its constitutive autophosphorylation and affects migration, invasion and proliferation of glioblastoma cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Systematic Review of Molecular Targeted Therapies for Adult-Type Diffuse Glioma: An Analysis of Clinical and Laboratory Studies.International journal of molecular sciences · 2023Pooled it
- Molecular Engineering of Aptamers for Glioblastoma Therapy: From Simple Antagonists to AI-Driven Approaches, a Narrative Review.International journal of molecular sciences · 2026Review
- Aptamers Structure Flexibility Is Crucial to EGFR Inhibition Function.Pharmaceuticals (Basel, Switzerland) · 2026Article
- EGFRvIII expression in head and neck squamous cell carcinoma: clinical significance and sources of frequency variation across studies.Frontiers in oncology · 2026Review
- Innovative aptamer approaches in glial tumor diagnostics and therapy: Progress and future directions.Molecular therapy. Nucleic acids · 2025Review
- A novel CD44-targeting aptamer recognizes chemoresistant mesenchymal stem-like TNBC cells and inhibits tumor growth.Bioactive materials · 2025Article
- In Vivo Evaluation ofPharmaceutics · 2024Article
- Gedunin modulates cellular growth and apoptosis in glioblastoma cell lines.Cancer reports (Hoboken, N.J.) · 2024Article
- Bispecific aptamer-decorated and light-triggered nanoparticles targeting tumor and stromal cells in breast cancer derived organoids: implications for precision phototherapies.Journal of experimental & clinical cancer research : CR · 2024Article
- Aptamers in neuro-oncology: An emerging therapeutic modality.Neuro-oncology · 2024Review
- Molecular Targeted Therapies in Glioblastoma Multiforme: A Systematic Overview of Global Trends and Findings.Brain sciences · 2023Review
- Review
- Article
- NF-κB in neurodegenerative diseases: Recent evidence from human genetics.Frontiers in molecular neuroscience · 2022Review
- Profiling Cancer Cells by Cell-SELEX: Use of Aptamers for Discovery of Actionable Biomarkers and Therapeutic Applications Thereof.Pharmaceutics · 2021Review
- Optimizing cisplatin delivery to triple-negative breast cancer through novel EGFR aptamer-conjugated polymeric nanovectors.Journal of experimental & clinical cancer research : CR · 2021Article
- Aptamers and antibodies: rivals or allies in cancer targeted therapy?Exploration of targeted anti-tumor therapy · 2021Review
- Aptamer-Based In Vivo Therapeutic Targeting of Glioblastoma.Molecules (Basel, Switzerland) · 2020Review
- Aptamer targeted therapy potentiates immune checkpoint blockade in triple-negative breast cancer.Journal of experimental & clinical cancer research : CR · 2020Article
- The Role of RNA and DNA Aptamers in Glioblastoma Diagnosis and Therapy: A Systematic Review of the Literature.Cancers · 2020Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma Multiforme (GBM) is the most common and aggressive human brain tumor, associated with very poor survival despite surgery, radiotherapy and chemotherapy.The epidermal growth factor receptor (EGFR) and the platelet-derived growth factor receptor β (PDGFRβ) are hallmarks in GBM with driving roles in tumor progression. In approximately half of the tumors with amplified EGFR, the EGFRvIII truncated extracellular mutant is detected. EGFRvIII does not bind ligands, is highly oncogenic and its expression confers resistance to EGFR tyrosine kinase inhibitors (TKIs). It has been demonstrated that EGFRvIII-dependent cancers may escape targeted therapy by developing dependence on PDGFRβ signaling, thus providing a strong rationale for combination therapy aimed at blocking both EGFRvIII and PDGFRβsignaling.We have recently generated two nuclease resistant RNA aptamers, CL4 and Gint4.T, as high affinity ligands and inhibitors of the human wild-type EGFR (EGFRwt) and PDGFRβ, respectively.Herein, by different approaches, we demonstrate that CL4 aptamer binds to the EGFRvIII mutant even though it lacks most of the extracellular domain. As a consequence of binding, the aptamer inhibits EGFRvIII autophosphorylation and downstream signaling pathways, thus affecting migration, invasion and proliferation of EGFRvIII-expressing GBM cell lines.Further, we show that targeting EGFRvIII by CL4, as well as by EGFR-TKIs, erlotinib and gefitinib, causes upregulation of PDGFRβ. Importantly, CL4 and gefitinib cooperate with the anti-PDGFRβ Gint4.T aptamer in inhibiting cell proliferation.The proposed aptamer-based strategy could have impact on targeted molecular cancer therapies and may result in progresses against GBMs.
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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.