Fragmentation level determines mitochondrial damage response and subsequently the fate of cancer cells exposed to carbon ions
文献类型：期刊论文
| 作者 | Li, Qiang ; Shen, Guosheng; Liu, Xiongxiong; Li, Ping; Hirayama, Ryoichi; Li, Hongbin; Liu, Bingtao; Li, Feifei; Zheng, Xiaogang; Jin, Xiaodong
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| 刊名 | RADIOTHERAPY AND ONCOLOGY
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| 出版日期 | 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 |
| WOS关键词 | DYNAMIN-RELATED PROTEIN-1 ; OXIDATIVE STRESS ; CYTOPLASMIC IRRADIATION ; TUMOR-CELLS ; DNA-DAMAGE ; FISSION ; AUTOPHAGY ; MITOPHAGY ; FUSION ; APOPTOSIS |
| 资助项目 | National Natural Science Foundation of China[11075191] ; National Natural Science Foundation of China[11205217] |
| WOS研究方向 | Oncology ; Radiology, Nuclear Medicine & Medical Imaging |
| 语种 | 英语 |
| WOS记录号 | WOS:000449458600012 |
| 出版者 | ELSEVIER IRELAND LTD |
| 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. |
入库方式： OAI收割
来源：近代物理研究所
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