| Project/Area Number |
15K08102
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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 |
Medical pharmacy
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| Research Institution | Daiichi University, College of Pharmaceutical Sciences (2017)
University of Miyazaki (2015-2016) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
青山 隆夫 東京理科大学, 薬学部薬学科, 教授 (60262028)
河野 洋平 東京理科大学, 薬学部薬学科, 助教 (80779025)
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| Research Collaborator |
OKUMURA MANABU
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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 |
¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2017: ¥260,000 (Direct Cost: ¥200,000、Indirect Cost: ¥60,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | カフェイン / シスプラチン / 肝細胞癌 / 肝細胞がん / アポトーシス / DNA修復 / 細胞増殖抑制 / 肝臓がん / 化学療法 |
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| Outline of Final Research Achievements |
Caffeine inhibits the proliferation of HCC cells by suppressing cell cycle progression without causing cell death. In combination therapy with caffeine and cisplatin, caffeine inhibits the ATM pathway activated by cisplatin, and the process of DNA repair is interfered with. Caffeine also inhibits the cisplatin-activated Akt pathway, and inhibits the functional molecules suppressing mitochondria-dependent cell death. These two functions of caffeine will likely enhance the cell death effect caused by cisplatin, and the interaction of caffeine with cisplatin would be primarily through the pharmacodynamic mechanism. However, HepG2 showed resistance to the enhancer action of caffeine. It will be necessary to investigate the mechanism of resistance to the action of caffeine in the future.
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