| Project/Area Number |
22K20795
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Multi-year Fund |
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| Review Section |
0901:Oncology and related fields
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| Research Institution | Nagasaki University |
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Principal Investigator |
YAN Chen 長崎大学, 原爆後障害医療研究所, 講師 (70968396)
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| Project Period (FY) |
2022-08-31 – 2024-03-31
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| Project Status |
Discontinued (Fiscal Year 2023)
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| Budget Amount *help |
¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2023: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2022: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | Radioresistance / Mitophagy / Cancer |
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| Outline of Research at the Start |
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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| Outline of Annual Research Achievements |
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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