Molecular mechanism of radio-sensitization by redox modification in cancer cells
| Project/Area Number |
15K09991
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Radiation science
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| Research Institution | University of Toyama |
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Principal Investigator |
ZHAO QING-LI 富山大学, 大学院医学薬学研究部(医学), 助教 (90313593)
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| Research Collaborator |
Li Peng
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 細胞死 / 放射線 / 温熱 |
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| Outline of Final Research Achievements |
In this study, the efficacy of some compounds was investigated to modify radiation or hyperthermia induced cell death. Lysolipin I or BU-4664L induced apoptosis in U937 and Molt-4 cells. In addition, Lisolipin I also enhanced radiation-induced apoptosis while, the low concentration BU-4664L have a protecting effect on radiation induced apoptosis. In this study, we determined that Tempo combine treatment with hyperthermia rapidly induced autophagic cell death. Tempo 5 mM -44℃/20 min combination induced apoptosis, while Tempo 5 mM -44℃/60 min combination induced autophagic cell death in HeLa cells. This co-treatment inhibited the processing of heat-activated procaspase-3 into active small subunits, leading to the inhibition of caspase-dependent apoptosis, and results in the induction of autophagic cell death. Furthermore, the gene chip analysis showed the up-regulation of TP53INP1 and cyclin-dependent kinase inhibitor (CDKI) genes in the combination treatment.
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Report
(4 results)
Research Products
(5 results)
