| 研究課題/領域番号 |
22K20795
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| 研究種目 |
研究活動スタート支援
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| 配分区分 | 基金 |
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| 審査区分 |
0901:腫瘍学およびその関連分野
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| 研究機関 | 長崎大学 |
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研究代表者 |
YAN Chen 長崎大学, 原爆後障害医療研究所, 講師 (70968396)
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| 研究期間 (年度) |
2022-08-31 – 2024-03-31
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| 研究課題ステータス |
中途終了 (2023年度)
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| 配分額 *注記 |
2,860千円 (直接経費: 2,200千円、間接経費: 660千円)
2023年度: 1,430千円 (直接経費: 1,100千円、間接経費: 330千円)
2022年度: 1,430千円 (直接経費: 1,100千円、間接経費: 330千円)
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| キーワード | Radioresistance / Mitophagy / Cancer |
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| 研究開始時の研究の概要 |
Radioresistance is one of the problems for cancer radiotherapy. Here we will investigate the role and mechanism of mitophagy on regulating radiation-induced ROS generation, CSCs plasticity and radioresistance. Data from this study will provide new insight on the mechanisms of radioresistance.
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| 研究実績の概要 |
Using human colorectal cancer cell lines (HCT116 and HCT8) for experiments, we found that 5Gy X-rays irradiation enhanced mitophagy activity and the expression of several mitophagy receptors (OPTN, BNIP3 and BNIP3L). Western blot analysis showed that the knockdown of BNIP3L enhanced the expression of γH2AX in HCT8 cells but not in HCT116 cells. However, the inhibition of mitophagy activity by either pharmacological mitophagy inhibitor Mdivi-1 or the knockdown of some mitophagy receptors did not significantly change the surviving fraction of HCT116 and HCT8 cells after radiation exposure. Our results suggest that mitophagy is responsible to ionizing radiation but may not play an important role on the radiosensitivity of cancer cells.
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