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Small-Molecule Inhibitors Targeting DNA Repair and DNA Repair Deficiency in Research and Cancer Therapy
Journal article   Open access   Peer reviewed

Small-Molecule Inhibitors Targeting DNA Repair and DNA Repair Deficiency in Research and Cancer Therapy

Sarah R. Hengel, M. Ashley Spies and Maria Spies
CELL CHEMICAL BIOLOGY, Vol.24(9), pp.1101-1119
09/21/2017
DOI: 10.1016/j.chembiol.2017.08.027
PMCID: PMC5679738
PMID: 28938088
url
https://doi.org/10.1016/j.chembiol.2017.08.027View
Published (Version of record) Open Access

Abstract

To maintain stable genomes and to avoid cancer and aging, cells need to repair a multitude of deleterious DNA lesions, which arise constantly in every cell. Processes that support genome integrity in normal cells, however, allow cancer cells to develop resistance to radiation and DNA-damaging chemotherapeutics. Chemical inhibition of the key DNA repair proteins and pharmacologically induced synthetic lethality have become instrumental in both dissecting the complex DNA repair networks and as promising anticancer agents. The difficulty in capitalizing on synthetically lethal interactions in cancer cells is that many potential targets do not possess well-defined small-molecule binding determinates. In this review, we discuss several successful campaigns to identify and leverage small-molecule inhibitors of the DNA repair proteins, from PARP1, a paradigm case for clinically successful small-molecule inhibitors, to coveted new targets, such as RAD51 recombinase, RAD52 DNA repair protein, MRE11 nuclease, and WRN DNA helicase.
Biochemistry & Molecular Biology Life Sciences & Biomedicine Science & Technology

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