Fragmentation level determines mitochondrial damage response and subsequently the fate of cancer cells exposed to carbon ions

doi:10.1016/j.radonc.2017.11.019

CORC > 近代物理研究所 > 中国科学院近代物理研究所 > 兰州重离子研究装置

	Fragmentation level determines mitochondrial damage response and subsequently the fate of cancer cells exposed to carbon ions
	Li, Qiang; Shen, Guosheng; Liu, Xiongxiong; Li, Ping; Hirayama, Ryoichi; Li, Hongbin; Liu, Bingtao; Li, Feifei; Zheng, Xiaogang; Jin, Xiaodong
刊名	RADIOTHERAPY AND ONCOLOGY
	2018
卷号	129 页码:75-83
关键词	Mitochondrial fragmentation Mitophagy Mitochondrion-mediated apoptosis Autophagy High-LET carbon ion radiation
ISSN号	0167-8140
DOI	10.1016/j.radonc.2017.11.019
英文摘要	Objectives: Although mitochondria are known to play an important role in radiation-induced cellular damage response, the mechanisms of how radiation elicits mitochondrial responses are largely unknown.Materials and methods: Human cervical cancer cell line HeLa and human breast cancer cell lines MCF-7 and MDA-MB-231 were irradiated with high LET carbon ions at low (0.5 Gy) and high (3 Gy) doses. Mitochondrial functions, dynamics, mitophagy, intrinsic apoptosis and total apoptosis, and survival fraction were investigated after irradiation.Results: We found that carbon ions irradiation induced two different mitochondrial morphological changes and corresponding responses in cancer cells. Cells exposed to carbon ions of 0.5 Gy exhibited only modestly truncated mitochondria, and subsequently damaged mitochondria could be eliminated through mitophagy. In contrast, mitochondria within cells insulted by 3 Gy radiation split into punctate and clustered ones, which were associated with apoptotic cell death afterward. Inhibition of mitochondrial fission by Drp1 or FIS1 knockdown or with the Drp1 inhibitor mdivi-1 suppressed mitophagy and potentiated apoptosis after irradiation at 0.5 Gy. However, inhibiting fission led to mitophagy and increased cell survival when cells were irradiated with carbon ions at 3 Gy.Conclusion: We proposed a stress response model to provide a mechanistic explanation for the mitochondrial damage response to high-LET carbon ions. (C) 2017 Elsevier B. V. All rights reserved. Radiotherapy and Oncology
资助项目	National Natural Science Foundation of China[11075191] ; National Natural Science Foundation of China[11205217]
WOS关键词	DYNAMIN-RELATED PROTEIN-1 ; OXIDATIVE STRESS ; CYTOPLASMIC IRRADIATION ; TUMOR-CELLS ; DNA-DAMAGE ; FISSION ; AUTOPHAGY ; MITOPHAGY ; FUSION ; APOPTOSIS
WOS研究方向	Oncology ; Radiology, Nuclear Medicine & Medical Imaging
语种	英语
出版者	ELSEVIER IRELAND LTD
WOS记录号	WOS:000449458600012
内容类型	期刊论文
源URL	[http://119.78.100.186/handle/113462/59886]
专题	近代物理研究所_兰州重离子研究装置近代物理研究所_生物物理研究室
通讯作者	Li, Qiang
作者单位	中国科学院近代物理研究所
推荐引用方式 GB/T 7714	Li, Qiang,Shen, Guosheng,Liu, Xiongxiong,et al. Fragmentation level determines mitochondrial damage response and subsequently the fate of cancer cells exposed to carbon ions[J]. RADIOTHERAPY AND ONCOLOGY,2018,129:75-83.
APA	Li, Qiang.,Shen, Guosheng.,Liu, Xiongxiong.,Li, Ping.,Hirayama, Ryoichi.,...&Jin, Xiaodong.(2018).Fragmentation level determines mitochondrial damage response and subsequently the fate of cancer cells exposed to carbon ions.RADIOTHERAPY AND ONCOLOGY,129,75-83.
MLA	Li, Qiang,et al."Fragmentation level determines mitochondrial damage response and subsequently the fate of cancer cells exposed to carbon ions".RADIOTHERAPY AND ONCOLOGY 129(2018):75-83.