ArticleMolecular therapy. Nucleic acids2022
An optimized MNK1b aptamer, apMNKQ2, and its potential use as a therapeutic agent in breast cancer.
Article in Molecular therapy. Nucleic acids, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 13 citations in OpenAlex.
- Aptamer-based inhibition of MNK1 reduces pancreatic ductal adenocarcinoma growth by targeting cancer stem cells.Journal of biomedical science · 2026Article
- Evolution and Trends of Aptamers in Cancer Research: A Bibliometric Analysis of the Literature over the Last Decade.Current medicinal chemistry · 2025Article
- Cationic Carbosilane Dendrimers for Apmnkq2 Aptamer Transfection in Breast Cancer: An Alternative to Traditional Transfectants.Macromolecular bioscience · 2025Article
- Current developments of SELEX technologies and prospects in the aptamer selection with clinical applications.Journal, genetic engineering & biotechnology · 2024Review
- An Aptamer against MNK1 for Non-Small Cell Lung Cancer Treatment.Pharmaceutics · 2023Article
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Authors and funding
17 authors at 4 institutions in 1 country.
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Abstract
Breast cancer is the most commonly diagnosed and leading cause of cancer death among women worldwide. Mitogen-activated protein kinase-interacting kinases (MNKs) promote the expression of several oncogenic proteins and are overexpressed in several types of cancer. In human cells, there are four isoforms of MNKs. The truncated isoform MNK1b, first described in our laboratory, has a higher basal activity and is constitutively active. Aptamers are emerging in recent years as potential therapeutic agents that show significant advantages over drugs of other nature. We have previously obtained and characterized a highly specific aptamer against MNK1b, named apMNK2F, with a dissociation constant in the nanomolar range, which produces significant inhibition of proliferation, migration, and colony formation in breast cancer cells. Furthermore, its sequence analysis predicted two G-quadruplex structures. In this work, we show the optimization process of the aptamer to reduce its size, improving its stability. The obtained aptamer, named apMNKQ2, is able to inhibit proliferation, colony formation, migration, and invasion in breast cancer cells. In murine models of breast cancer, apMNKQ2 has demonstrated its efficacy in reducing tumor volume and the number of metastases. In conclusion, apMNKQ2 could be used as an anti-tumor drug in the future.
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