ArticleMolecular therapy. Nucleic acids2023
Combination of protein and cell internalization SELEX identifies a potential RNA therapeutic and delivery platform to treat EphA2-expressing tumors.
Article in Molecular therapy. Nucleic acids, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Are we there yet with XNA aptamers?RSC advances · 2026Review
- From randomness to recognition: modeling the evolution of DNA sequence information during enrichment for binding.Bioinformatics advances · 2026Article
- AptamerRunner: An accessible aptamer structure prediction and clustering algorithm for visualization of selected aptamers.Molecular therapy. Nucleic acids · 2024Article
- Current developments of SELEX technologies and prospects in the aptamer selection with clinical applications.Journal, genetic engineering & biotechnology · 2024Review
- AptamerRunner: An accessible aptamer structure prediction and clustering algorithm for visualization of selected aptamers.bioRxiv : the preprint server for biology · 2023Article
- Aptamers as Potential Therapeutic Tools for Ovarian Cancer: Advancements and Challenges.Cancers · 2023Review
- Combining independent protein and cellular SELEX with bioinformatic analysis may allow high affinity aptamer hit discovery.Molecular therapy. Nucleic acids · 2023Article
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
The EphA2 receptor tyrosine kinase is overexpressed in most solid tumors and acts as the major driver of tumorigenesis. In this study, we developed a novel approach for targeting the EphA2 receptor using a 2'-fluoro-modified pyrimidine RNA aptamer termed ATOP. We identified the ATOP EphA2 aptamer using a novel bioinformatics strategy that compared aptamers enriched during a protein SELEX using recombinant human EphA2 and a cell-internalization SELEX using EphA2-expressing MDA231 tumor cells. When applied to EphA2-expressing tumor cell lines, the ATOP EphA2 aptamer attenuated tumor cell migration and clonogenicity. In a mouse model of spontaneous metastasis, the ATOP EphA2 aptamer slowed primary tumor growth and significantly reduced the number of lung metastases. The EphA2 ATOP aptamer represents a promising candidate for the development of next-generation targeted therapies that provide safer and more effective treatment of EphA2-overexpressing tumors.
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