High LET Radiation Enhances Nocodazole Induced Cell Death in HeLa Cells through Mitotic Catastrophe and Apoptosis
文献类型:期刊论文
作者 | Furusawa, Yoshiya2; Li, Qiang1,3![]() ![]() ![]() ![]() ![]() ![]() |
刊名 | JOURNAL OF RADIATION RESEARCH
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出版日期 | 2011-07-01 |
卷号 | 52页码:481-489 |
关键词 | HeLa cells Nocodazole High LET radiation Mitotic catastrophe Apoptosis |
ISSN号 | 0449-3060 |
DOI | 10.1269/jrr.10186 |
英文摘要 | To understand how human tumor cells respond to the combined treatment with nocodazole and high LET radiation, alterations in cell cycle, mitotic disturbances and cell death were investigated in the present study. Human cervix carcinoma HeLa cells were exposed to nocodazole for 18 h immediately followed by high LET iron ion irradiation and displayed a sequence of events leading to DNA damages, mitotic aberrations, interphase restitution and endocycle as well as cell death. A prolonged mitotic arrest more than 10 h was observed following nocodazole exposure, no matter the irradiation was present or not. The occurrence of mitotic slippage following the mitotic arrest was only drug-dependent and the irradiation did not accelerate it. The amount of polyploidy cells was increased following mitotic slippage. No detectable G(2) or G(1) arrest was observed in cells upon the combined treatment and the cells reentered the cell cycle still harboring unrepaired cellular damages. This premature entry caused an increase of multipolar mitotic spindles and amplification of centrosomes, which gave rise to lagging chromosomal material, failure of cytokinesis and polyploidization. These mitotic disturbances and their outcomes confirmed the incidence of mitotic catastrophe and delayed apoptotic features displayed by TUNEL method after the combined treatment. These results suggest that the addition of high-LET iron ion irradiation to nocodazole enhanced mitotic catastrophe and delayed apoptosis in HeLa cells. These might be important cell death mechanisms involved in tumor cells in response to the treatment of antimitotic drug combined with high LET radiation. |
WOS关键词 | SPINDLE-ASSEMBLY CHECKPOINT ; HEAVY-ION RADIATION ; DNA-DAMAGE ; IONIZING-RADIATION ; X-RAYS ; ARREST ; P53 ; CYTOKINESIS ; IRRADIATION ; MECHANISMS |
资助项目 | National Basic Research Program of China (973 Program)[2010CB834203] ; National Natural Science Foundation of China[10835011] ; National Natural Science Foundation of China[10905080] ; National Natural Science Foundation of China[11075191] ; Science and Technology Development Project of Lanzhou City[2008-sr-10] ; Science and Technology Development Project of Lanzhou City[2009-2-12] |
WOS研究方向 | Life Sciences & Biomedicine - Other Topics ; Radiology, Nuclear Medicine & Medical Imaging |
语种 | 英语 |
WOS记录号 | WOS:000294885200011 |
出版者 | JAPAN RADIATION RESEARCH SOC |
资助机构 | National Basic Research Program of China (973 Program) ; National Natural Science Foundation of China ; Science and Technology Development Project of Lanzhou City |
源URL | [http://ir.impcas.ac.cn/handle/113462/18588] ![]() |
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, Qiang |
作者单位 | 1.Chinese Acad Sci, Inst Modern Phys, Lanzhou 730000, Peoples R China 2.Natl Inst Radiol Sci, Heavy Ion Radiobiol Res Grp, Chiba 2638555, Japan 3.Chinese Acad Sci, Key Lab Heavy Ion Radiat Biol & Med, Lanzhou 730000, Peoples R China 4.Chinese Acad Sci, Grad Sch, Beijing 100039, Peoples R China |
推荐引用方式 GB/T 7714 | Furusawa, Yoshiya,Li, Qiang,Li, Ping,et al. High LET Radiation Enhances Nocodazole Induced Cell Death in HeLa Cells through Mitotic Catastrophe and Apoptosis[J]. JOURNAL OF RADIATION RESEARCH,2011,52:481-489. |
APA | Furusawa, Yoshiya.,Li, Qiang.,Li, Ping.,Zhou, Libin.,Dai, Zhongying.,...&Matsumoto, Yoshitaka.(2011).High LET Radiation Enhances Nocodazole Induced Cell Death in HeLa Cells through Mitotic Catastrophe and Apoptosis.JOURNAL OF RADIATION RESEARCH,52,481-489. |
MLA | Furusawa, Yoshiya,et al."High LET Radiation Enhances Nocodazole Induced Cell Death in HeLa Cells through Mitotic Catastrophe and Apoptosis".JOURNAL OF RADIATION RESEARCH 52(2011):481-489. |
入库方式: OAI收割
来源:近代物理研究所
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