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Fragmentation level determines mitochondrial damage response and subsequently the fate of cancer cells exposed to carbon ions.
https://repo.qst.go.jp/records/49291
https://repo.qst.go.jp/records/49291cc0d45a3-c3a5-48b4-99d8-80699106d1a1
| Item type | 学術雑誌論文 / Journal Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2018-11-30 | |||||
| タイトル | ||||||
| タイトル | Fragmentation level determines mitochondrial damage response and subsequently the fate of cancer cells exposed to carbon ions. | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 著者 |
Jin, Xiaodong
× Jin, Xiaodong× Zheng, Xiaogang× Li, Feifei× Liu, Bingtao× Li, Hongbin× Hirayama, Ryoichi× Li, Ping× Liu, Xiongxiong× Shen, Guosheng× Li, Qiang× Jin, Xiaodong× Hirayama, Ryoichi× Li, Ping× Xiongxiong, Liu× Li, Qiang |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | 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. |
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| 書誌情報 |
Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology 巻 129, 号 1, p. 75-83, 発行日 2018-10 |
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| 出版者 | ||||||
| 出版者 | Elsevier Scientific Publishers | |||||
| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 0167-8140 | |||||
| PubMed番号 | ||||||
| 識別子タイプ | PMID | |||||
| 関連識別子 | 29208514 | |||||
| DOI | ||||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1016/j.radonc.2017.11.019 | |||||
