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Mitotic DNA damages induced by carbon-ion radiation incur additional chromosomal breaks in polyploidy

文献类型：期刊论文

作者Liu, XG11; Ye, F11; Zhao, T11; Jin, XD11; Liu, XX11; Li, P11; Zhou, LB11; Li, Q (reprint author), Chinese Acad Sci, Inst Modern Phys, 509 Nanchang Rd, Lanzhou 730000, Peoples R China.; Li, Q11; Hirayama, R11
刊名TOXICOLOGY LETTERS
出版日期2014
卷号230页码:36-47
关键词Induced Cell-death Histone H2ax Cancer-cells Mammalian-cells Tumor-cells Apoptosis Catastrophe P53 Phosphorylation Irradiation
ISSN号0378-4274
DOI10.1016/j.toxlet.2014.08.006
英文摘要Compared with low linear energy transfer (LET) radiation, carbon-ion radiation has been proved to induce high frequency of more complex DNA damages, including DNA double strands (DSBs) and non-DSB clustered DNA lesions. Chemotherapeutic drug doxorubicin has been reported to elicit additional H2AX phosphorylation in polyploidy. Here, we investigated whether mitotic DNA damage induced by high-LET carbon-ion radiation could play the same role. We demonstrate that impairment of post-mitotic G(1) and S arrest and abrogation of post-mitotic G(2)-M checkpoint failed to prevent mis-replication of damaged DNA and mis-separation of chromosomes. Meanwhile, mitotic slippage only nocodazole-related, cytokinesis failure and cell fusion collectively contributed to the formation of binucleated cells. Chk1 and Cdh1 activation was inhibited when polyploidy emerged in force, both of which are critical components for mitotic exit and cytokinesis. Carbon-ion radiation irrelevant of nocodazole incurred additional DNA breaks in polyploidy, manifesting as structural and numerical karyotype changes. The proliferation of cells given pre-synchronization and radiation was completely inhibited and cells were intensely apoptotic. Since increased chromosomal damage resulted in extensive H2AX phosphorylation during polyploidy, we propose that the additional gamma-H2AX during polyploidy incurred by carbon-ion radiation provides a final opportunity for these dangerous and chromosomally unstable cells to be eliminated. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
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WOS关键词INDUCED CELL-DEATH ; HISTONE H2AX ; CANCER-CELLS ; MAMMALIAN-CELLS ; TUMOR-CELLS ; APOPTOSIS ; CATASTROPHE ; P53 ; PHOSPHORYLATION ; IRRADIATION
资助项目Gansu Provincial Funds for Distinguished Young Scientists[1111RJDA010]
WOS研究方向Toxicology
语种英语
WOS记录号WOS:000341879900005
出版者ELSEVIER IRELAND LTD
资助机构National Basic Research Program of China (973 Program) [2010 CB834203] ; National Basic Research Program of China (973 Program) [2010 CB834203] ; National Natural Science Foundation of China [U1232207, 11205217, 11075191] ; National Natural Science Foundation of China [U1232207, 11205217, 11075191] ; Gansu Provincial Funds for Distinguished Young Scientists [1111RJDA010] ; Gansu Provincial Funds for Distinguished Young Scientists [1111RJDA010]
源URL[http://ir.impcas.ac.cn/handle/113462/18577]  
专题近代物理研究所_医学物理研究室
近代物理研究所_生物物理研究室
通讯作者Li, Q (reprint author), Chinese Acad Sci, Inst Modern Phys, 509 Nanchang Rd, Lanzhou 730000, Peoples R China.
作者单位1.Li, Feifei
2.[Furusawa, Yoshiya] Natl Inst Radiol Sci, Res Ctr Charged Particle Therapy, Chiba 260, Japan
3.Zheng, Xiaogang] Univ Chinese Acad Sci, Beijing, Peoples R China
4.Li, Feifei
5.Liu, Xiongxiong
6.Ye, Fei
7.[Liu, Yan
8.Li, Qiang] Chinese Acad Sci, Key Lab Heavy Ion Radiat Biol & Med, Lanzhou 730000, Gansu, Peoples R China
9.Dai, Zhongying
10.Zheng, Xiaogang
推荐引用方式
GB/T 7714		 Liu, XG,Ye, F,Zhao, T,et al. Mitotic DNA damages induced by carbon-ion radiation incur additional chromosomal breaks in polyploidy[J]. TOXICOLOGY LETTERS,2014,230:36-47.
APA Liu, XG.,Ye, F.,Zhao, T.,Jin, XD.,Liu, XX.,...&Hirayama, R.(2014).Mitotic DNA damages induced by carbon-ion radiation incur additional chromosomal breaks in polyploidy.TOXICOLOGY LETTERS,230,36-47.
MLA Liu, XG,et al."Mitotic DNA damages induced by carbon-ion radiation incur additional chromosomal breaks in polyploidy".TOXICOLOGY LETTERS 230(2014):36-47.

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来源：近代物理研究所

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