Santana Viera, LauraDassie, Justin P.Rosàs Lapeña, MartaGarcia Monclús, SilviaChicón Bosch, MarionaPérez Capó, MarinaPozo, Lidia delSánchez Serra, SaraAlmacellas Rabaiget, OlgaMaqueda Marcos, SusanaLópez Alemany, RoserThiel, William H.Giangrande, Paloma H.Tirado, Oscar M.2023-10-062023-10-062023-05-082162-2531https://hdl.handle.net/2445/202625The 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 20-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.15 p.application/pdfengcc by-nc-nd (c) Santana Viera, Laura et al., 2023http://creativecommons.org/licenses/by-nc-nd/3.0/es/Virus oncogènicsTerapèuticaOncogenic virusesTherapeuticsinfo:eu-repo/semantics/article2023-09-22info:eu-repo/semantics/openAccess37251690