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Targeting DNA mismatches with metal complexes

Natalia Kolozsvari, Martin Gill Orcid Logo

Journal of Inorganic Biochemistry, Volume: 271, Start page: 112977

Swansea University Authors: Natalia Kolozsvari, Martin Gill Orcid Logo

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Abstract

DNA mismatches are non Watson-Crick base pairs that arise from errors during replication or are the result of DNA damage. Normally repaired by the mismatch mediated repair (MMR) pathway, in cancers deficient in MMR, such as subsets of colorectal and endometrial cancers, mismatches persist and accumu...

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Published in: Journal of Inorganic Biochemistry
ISSN: 0162-0134 1873-3344
Published: Elsevier BV 2025
Online Access: Check full text

URI: https://cronfa.swan.ac.uk/Record/cronfa69837
Abstract: DNA mismatches are non Watson-Crick base pairs that arise from errors during replication or are the result of DNA damage. Normally repaired by the mismatch mediated repair (MMR) pathway, in cancers deficient in MMR, such as subsets of colorectal and endometrial cancers, mismatches persist and accumulate, providing a biochemical vulnerability creating a target for small-molecule intervention. This review explores how metal complexes employing rhodium(III), ruthenium(II) or platinum(II) centres can exploit this molecular distinction to preferentially bind mismatch sites in DNA. We discuss the potential of this interaction to act as a foundation for next-generation therapeutics and imaging probes where the unique structural, electronic, and photophysical properties of metal complexes and associated ligand design offer opportunities to differentiate between canonical and mismatched DNA with high selectivity.
Keywords: Rhodium; Ruthenium; Platinum; Mismatch DNA; cancer; MMR deficient
College: Faculty of Science and Engineering
Funders: This work was supported by Cancer Research Wales (Pritchard and Moore Scholarship, grant no. 2542).
Start Page: 112977