Cited by 1,220DNA Repair MechanismsEffects of Radiation ExposureProtein Kinase Regulation and GTPase Signaling

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Identification and Characterization of a Novel and Specific Inhibitor of the Ataxia-Telangiectasia Mutated Kinase ATM

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Hickson, Ian, Zhao, Yan, Richardson, Caroline J., Green, Sharon J., Martin, Niall M. B., Orr, Alisdair I., Reaper, Philip M., Jackson, Stephen P., Curtin, Nicola J., Smith, Graeme C. M.·2004·Cancer Research

DOI 10.1158/0008-5472.can-04-2727

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Abstract

The serine/threonine protein kinase ATM signals to cell cycle and DNA repair components by phosphorylating downstream targets such as p53, CHK2, NBS1, and BRCA1. Mutation of ATM occurs in the human autosomal recessive disorder ataxia-telangiectasia, which is characterized by hypersensitivity to ionizing radiation and a failure of cells to arrest the cell cycle after the induction of DNA double-strand breaks. It has thus been proposed that ATM inhibition would cause cellular radio- and chemosensitization. Through screening a small molecule compound library developed for the phosphatidylinositol 3'-kinase-like kinase family, we identified an ATP-competitive inhibitor, 2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one (KU-55933), that inhibits ATM with an IC(50) of 13 nmol/L and a Ki of 2.2 nmol/L. KU-55933 shows specificity with respect to inhibition of other phosphatidylinositol 3'-kinase-like kinases. Cellular inhibition of ATM by KU-55933 was demonstrated by the ablation of ionizing radiation-dependent phosphorylation of a range of ATM targets, including p53, gammaH2AX, NBS1, and SMC1. KU-55933 did not show inhibition of UV light DNA damage induced cellular phosphorylation events. Exposure of cells to KU-55933 resulted in a significant sensitization to the cytotoxic effects of ionizing radiation and to the DNA double-strand break-inducing chemotherapeutic agents, etoposide, doxorubicin, and camptothecin. Inhibition of ATM by KU-55933 also caused a loss of ionizing radiation-induced cell cycle arrest. By contrast, KU-55933 did not potentiate the cytotoxic effects of ionizing radiation on ataxia-telangiectasia cells, nor did it affect their cell cycle profile after DNA damage. We conclude that KU-55933 is a novel, specific, and potent inhibitor of the ATM kinase.

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Authors: Hickson, I., Zhao, Y., Richardson, C. J., Green, S. J., Martin, N. M. B., Orr, A. I., Reaper, P. M., Jackson, S. P., Curtin, N. J., & Smith, G. C. M.
Affiliations: 1KuDOS Pharmaceuticals Ltd., Cambridge Science Park, Milton Road, Cambridge;
Newcastle University (GB)
University of Cambridge (GB)
ORCID: Hickson, Ian
Zhao, Yan
Martin, Niall M. B.
Jackson, Stephen P.
Curtin, Nicola J.
Smith, Graeme C. M.
Venue: Cancer Research
Publisher: American Association for Cancer Research (AACR)
Published: 2004-12-15
Volume: 64
Issue: 24
Pages: 9152-9159
ISSN: 0008-5472 (ISSN-L)
1538-7445
DOI: 10.1158/0008-5472.can-04-2727
OpenAlex: W2101988823
Cited by: 1,220
References: 58
Citations by year: 2026: 26 · 2025: 31 · 2024: 38 · 2023: 49 · 2022: 31 · 2021: 32 · 2020: 53 · 2019: 55 · 2018: 48 · 2017: 66 · 2016: 71 · 2015: 76 · 2014: 70 · 2013: 62 · 2012: 92
FWCI: 11.39
Type: journal article
Language: en
Open access: green
doi.org
Locations: Cancer Research (publishedVersion)
PubMed (publishedVersion)
Newcastle University ePrints (Newcastle Univesity)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Keywords: ATM kinase, KU55933, kinase inhibitors, ataxia telangiectasia, radiosensitivity, DNA double-strand breaks, cell cycle arrest, p53 phosphorylation, NBS1, radiosensitization, chemosensitization, etoposide, doxorubicin, camptothecin, γH2AX, SMC1A
MeSH terms: Cell Cycle, Chromones, DNA-Binding Proteins, HeLa Cells, Humans, Kinetics, Morpholines, Phosphorylation, Pyrones, Radiation-Sensitizing Agents, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Inhibitory Concentration 50, Combinatorial Chemistry Techniques, Tumor Suppressor Proteins, Cell Line, Tumor, Protein Kinase Inhibitors, Ataxia Telangiectasia Mutated Proteins

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Identification and Characterization of a Novel and Specific Inhibitor of the Ataxia-Telangiectasia Mutated Kinase ATM

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