ArticleScientific reports2017
Aptamer-mediated impairment of EGFR-integrin αvβ3 complex inhibits vasculogenic mimicry and growth of triple-negative breast cancers.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 93 citations in OpenAlex.
- Synergistic Regulation of Tumor Immunity by Integrins and Lectins: From Molecular Mechanisms to Dual-Targeted Therapy.International journal of molecular sciences · 2026Review
- Angiocrine factors in tumor microenvironment: bidirectional crosstalk, mechanistic insights, and therapeutic strategies.Journal of translational medicine · 2026Review
- A novel CD44-targeting aptamer recognizes chemoresistant mesenchymal stem-like TNBC cells and inhibits tumor growth.Bioactive materials · 2025Article
- Triple-Negative Breast Cancer Progression and Drug Resistance in the Context of Epithelial-Mesenchymal Transition.Cancers · 2025Review
- Breaking the bottlenecks in anti-tumor angiogenic therapy: targeting vasculogenic mimicry with natural products and traditional Chinese medicine.Frontiers in pharmacology · 2025Review
- The solid tumor microenvironment and related targeting strategies: a concise review.Frontiers in immunology · 2025Review
- Engineered in vivo and in vitro tumor model recapitulates vasculogenic mimicry signatures in melanoma.Bioengineering & translational medicine · 2024Article
- Recent Progress of Multifunctional Molecular Probes for Triple-Negative Breast Cancer Theranostics.Pharmaceutics · 2024Review
- 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
- Mechanisms of angiogenesis in tumour.Frontiers in oncology · 2024Review
- SNORD17-mediated KAT6B mRNA 2'-O-methylation regulates vasculogenic mimicry in glioblastoma cells.Cell biology and toxicology · 2023Article
- Targeting triple-negative breast cancer cells with a β1-integrin binding aptamer.Molecular therapy. Nucleic acids · 2023Article
- Article
- Targeting cancer stem cell plasticity in triple-negative breast cancer.Exploration of targeted anti-tumor therapy · 2023Review
- Physicochemical aspects of the tumour microenvironment as drivers of vasculogenic mimicry.Cancer metastasis reviews · 2022Review
- Advances in Aptamers-Based Applications in Breast Cancer: Drug Delivery, Therapeutics, and Diagnostics.International journal of molecular sciences · 2022Review
- Luminal androgen receptor (LAR) subtype of triple-negative breast cancer: molecular, morphological, and clinical features.Journal of Zhejiang University. Science. B · 2022Review
- Metabolomics and EMT Markers of Breast Cancer: A Crosstalk and Future Perspective.Pathophysiology : the official journal of the International Society for Pathophysiology · 2022Review
- m6A methylated EphA2 and VEGFA through IGF2BP2/3 regulation promotes vasculogenic mimicry in colorectal cancer via PI3K/AKT and ERK1/2 signaling.Cell death & disease · 2022Article
- Optimization of Short RNA Aptamers for TNBC Cell Targeting.International journal of molecular sciences · 2022Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current treatment options for triple-negative breast cancers (TNBCs) is limited by the absence of well-defined biomarkers, excluding a targeted therapy. Notably, epidermal growth factor receptor (EGFR) is overexpressed in a great proportion of TNBCs and is a negative prognostic factor. In clinical trials, however, existing EGFR inhibitors showed disappointing outcome. Oligonucleotide aptamers are a valid alternative to antibodies for diagnostic and therapeutic uses. Here, we prove that, when applied to aggressive TNBC cell lines with unique stem-like plasticity, the anti-EGFR CL4 aptamer, but not erlotinib or cetuximab, prevents the vasculogenic mimicry (VM) capability of the cells and destroys previously formed channels in three-dimensional culture. Notably, we found that CL4 impairs the matrix-induced integrin αvβ3 interaction with EGFR and integrin αvβ3-dependent cell adhesion. Consistently, the aptamer strongly inhibits VM and tumor growth in a xenograft TNBC model. These data suggest that in TNBC cells, EGFR may cooperate with integrin αvβ3 to regulate integrin binding to extracellular ligands required for VM, and EGFR-targeting by CL4 aptamer may counteract this event. Overall, we demonstrate a novel mechanism of action for CL4 related with integrin αvβ3-EGFR interaction, that may help to develop new oligonucleotide-based strategy addressing unmet need for TNBCs therapy.
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