| Project/Area Number |
15K10711
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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 |
Obstetrics and gynecology
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| Research Institution | Shinshu University |
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Principal Investigator |
Asaka Ryoichi 信州大学, 学術研究院医学系(医学部附属病院), 助教 (00623688)
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| Co-Investigator(Kenkyū-buntansha) |
塩沢 丹里 信州大学, 学術研究院医学系, 教授 (20235493)
宮本 強 信州大学, 学術研究院医学系, 准教授 (70418721)
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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 |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | SIRT1 / サーチュイン / 子宮内膜癌 / 卵巣癌 / 抗がん剤耐性 / 癌幹細胞 / SIRT1阻害薬 / Sirtuin1 / 酸化ストレス耐性 / シスプラチン |
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| Outline of Final Research Achievements |
SIRT1 expression was enhanced in ovarian cancer tissues and the patients with strong expression of SIRT1 showed a poor prognosis. Cytotoxic stress caused by anticancer drugs and hydrogen peroxide enhanced the SIRT1 expression, suppression of SIRT1 expression attenuated the resistance against anticancer agents and forced-expression of SIRT1 enhanced that. Thus, SIRT1 may enhance the cell viability against cytotoxic stress such as anticancer drugs. SIRT1 promoted anchorage-independent colonization in soft agar and enhanced the expression of stemness-related genes such as Nanog. Thus, SIRT1 may act on stem cell maintenance and this function may also be involved in enhancing cell viability by SIRT1. The SIRT1 inhibitor, EX527, canceled the anchorage-independent colonization promoted by SIRT1 and enhanced the antitumor effect of cisplatin.
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