ArticleNucleic acids research2025
Targeting DNA termini with a small-molecule natural product analogue: a DNA end-binder (DEB) to augment DNA double-strand breaks.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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9 authors.
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Abstract
DNA double-strand breaks generate exposed DNA ends, which, if left unrepaired, can be highly deleterious. Eukaryotic cells have evolved multiple mechanisms to safeguard these DNA ends and maintain genomic integrity. This study screened synthetic natural product analogues to identify small-molecule ligands that selectively sequester broken DNA ends. A potential DNA end-binder (DEB) was serendipitously identified among discolin and bacillimidazole-based compounds. DEB interaction resulted in fluorescence quenching of ethidium bromide in linear but not circular DNA, indicating preferential binding to DNA termini. DEB inhibited exonucleases and ligases that bind DNA termini, forming a stable complex, as confirmed by gel retardation analysis. Molecular dynamics simulations revealed strong binding affinity at terminal base pairs through electrostatic, amphiphilic, and stacking interactions. When combined with Topo-II inhibitor epirubicin, the DEB enhanced DNA break accumulation and cytotoxicity in cancer cells. These findings introduce a new class of DNA end-specific small-molecule ligands with promising therapeutic potential.
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