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Combination of protein and cell internalization SELEX identifies a potential RNA therapeutic and delivery platform to treat EphA2 expressing tumors
Journal article   Open access   Peer reviewed

Combination of protein and cell internalization SELEX identifies a potential RNA therapeutic and delivery platform to treat EphA2 expressing tumors

Laura Santana-Viera, Justin P. Dassie, Marta Rosàs-Lapeña, Silvia Garcia-Monclús, Mariona Chicón-Bosch, Marina Pérez-Capó, Lidia del Pozo, Sara Sanchez-Serra, Olga Almacellas-Rabaiget, Susana Maqueda-Marcos, …
Molecular therapy. Nucleic acids, Vol.32, pp.P758-772
05/2023
DOI: 10.1016/j.omtn.2023.05.003
PMCID: PMC10213179
PMID: 37251690
url
https://doi.org/10.1016/j.omtn.2023.05.003View
Published (Version of record) Open Access

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. [Display omitted] Santana-Viera and colleagues developed a novel 2’F-Py RNA aptamer against EphA2 receptor using a combinatorial SELEX strategy. Its anti-tumorigenic properties shown in vitro and in vivo, put forward this aptamer as a promising candidate for the development of aptamer-based therapeutics towards the many tumors over-expressing EphA2.

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