Differences in Sensitivity to DNA-damaging Agents between XRCC4- and Artemis-deficient Human Cells (original) (raw)
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1Radiation Effect Mechanisms Research Group, Research Center for Radiation Protection
3Particle Radiation Molecular Biology Unit, International Open laboratory, National Institute of Radiological Sciences, 4-9-1 Anagawa, Inage-ku, Chiba-shi, Chiba 263-8555, Japan.
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1Radiation Effect Mechanisms Research Group, Research Center for Radiation Protection
3Particle Radiation Molecular Biology Unit, International Open laboratory, National Institute of Radiological Sciences, 4-9-1 Anagawa, Inage-ku, Chiba-shi, Chiba 263-8555, Japan.
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1Radiation Effect Mechanisms Research Group, Research Center for Radiation Protection
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2Radgenomics Research Group, Research Center for Charged Particle Therapy
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2Radgenomics Research Group, Research Center for Charged Particle Therapy
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1Radiation Effect Mechanisms Research Group, Research Center for Radiation Protection
3Particle Radiation Molecular Biology Unit, International Open laboratory, National Institute of Radiological Sciences, 4-9-1 Anagawa, Inage-ku, Chiba-shi, Chiba 263-8555, Japan.
*Corresponding author: Phone: +81-43-206-3128, Fax: +81-43-255-6819, E-mail: onoda@nirs.go.jp
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Note: Cell lines used in the current study will be available from CELL BANK in the RIKEN BIORESOURCE CENTER (Tsukuba, Ibaraki, Japan/E-mail: cellbank@brc.riken.jp).
Received:
25 November 2010
Revision received:
26 January 2011
Accepted:
07 February 2011
PDF Cite
Takanori Katsube, Masahiko Mori, Hideo Tsuji, Tadahiro Shiomi, Naoko Shiomi, Makoto Onoda, Differences in Sensitivity to DNA-damaging Agents between _XRCC4_- and _Artemis_-deficient Human Cells, Journal of Radiation Research, Volume 52, Issue 4, July 2011, Pages 415–424, https://doi.org/10.1269/jrr.10168
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Abstract
Non-homologous end-joining (NHEJ) is the predominant pathway for the repair of DNA double-strand breaks (DSBs) in human cells. XRCC4 is indispensable to NHEJ and functions together with DNA ligase IV in the rejoining of broken DNA ends. Artemis is a nuclease required for trimming of some, but not all, types of broken DNA ends prior to rejoining by the DNA ligase IV/XRCC4 complex. To better understand the roles of these factors, we generated _XRCC4_- and _Artemis_-deficient cells from the human colon adenocarcinoma cell line HCT116 by gene targeting and examined their cellular responses to several DNA-damaging agents including X-rays. As anticipated, kinetic analyses of γ-H2AX foci and chromosomal aberrations after ionizing radiation (IR) demonstrated a serious incompetence of DSB repair in the _XRCC4_-deficient cells, and relatively moderate impairment in the _Artemis_-deficient cells. The _XRCC4_-deficient cells were highly sensitive to etoposide and 5-fluoro-2'-deoxyuridine as well as IR, and moderately sensitive to camptothecin, methyl methanesulfonate, cisplatin, mitomycin C, aphidicolin and hydroxyurea, compared to the parental HCT116 cells. The _Artemis_-deficient cells were not as sensitive as the _XRCC4_-deficient cells, except to cisplatin and mitomycin C. By contrast, the _Artemis_-deficient cells were significantly more resistant to hydroxyurea than the parental cells. These observations suggest that Artemis also functions in some DNA damage response pathways other than NHEJ in human cells.
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Author notes
Note: Cell lines used in the current study will be available from CELL BANK in the RIKEN BIORESOURCE CENTER (Tsukuba, Ibaraki, Japan/E-mail: cellbank@brc.riken.jp).
Copyright © 2011 by Journal of Radiation Research Editorial Committee
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