| Project/Area Number |
21390504
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pathobiological dentistry/Dental radiology
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| Research Institution | Nagasaki University |
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Principal Investigator |
NAKAMURA Takashi 長崎大学, 大学院・医歯薬学総合研究科, 教授 (30172406)
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| Co-Investigator(Kenkyū-buntansha) |
SUMI Misa 長崎大学, 大学院・医歯薬学総合研究科, 准教授 (90284702)
HOTOKEZAKA Yuka 長崎大学, 大学病院, 講師 (10244089)
KIMURA Yasuo 長崎大学, 大学院・医歯薬学総合研究科, 助教 (30253686)
TASHIRO Shigeki 長崎大学, 大学院・医歯薬学総合研究科, 助教 (20300882)
SUMI Tadateru 長崎大学, 大学院・医歯薬学総合研究科, 助教 (80284701)
TAKAGI Yukinori 長崎大学, 大学院・医歯薬学総合研究科, 助教 (30295084)
EIDA Sato 長崎大学, 大学院・医歯薬学総合研究科, 助教 (80325662)
KATAYAMA Ikuo 長崎大学, 大学病院, 助教 (80295089)
SASAKI Miho 長崎大学, 大学病院, 助教 (10437874)
ICHIKAWA Youko 長崎大学, 大学病院, 助教 (90380857)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥18,200,000 (Direct Cost: ¥14,000,000、Indirect Cost: ¥4,200,000)
Fiscal Year 2011: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2009: ¥8,970,000 (Direct Cost: ¥6,900,000、Indirect Cost: ¥2,070,000)
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| Keywords | FEN1 / マウスモデル / 紫外線 / 腫瘍 / P53 / テロメア / DAN切断 / 細胞周期 / 老化促進 / DNA切断 |
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| Research Abstract |
Here we investigated the effects of FEN1 ablation on growth of different cell types with or without intact p53 by using RNA interference. We found that the FEN1 ablation triggers senescence in p53-mutated T24 cells. However, transfection of the wild-type p53 into these T24 cells inhibited the senescence. On the other hand, HT116 cells with the wild-type p53 were not introduced to senescence by interfering FEN1 expression ; instead, the cells underwent apoptosis. Contrary in HT116 cells defective of p53 did not exhibit senescence or apoptosis after FEN1 siRNA treatment. Interestingly, ionizing irradiation(5Gy) caused senescence in p53-dfective HT116 cells that were treated with FEN1 siRNA. These results suggest that FEN1-induced senescence is p53-dependent and imply that this mechanism may be involved in UV-induced tumorigenesis.
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