| Project/Area Number |
24592525
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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 | Nara Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KOBAYASHI Hiroshi 奈良県立医科大学, 医学部, 教授 (40178330)
YOSHIDA Syozo 奈良県立医科大学, 医学部, 助教 (40347555)
KAWAGUCHI Ryuji 奈良県立医科大学, 医学部, 助教 (50382289)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 卵巣明細胞腺癌 / HNF-1beta / チェックポイント / 卵巣子宮内膜症 / 癌化 / 細胞周期 / claspin |
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| Outline of Final Research Achievements |
Ovarian clear cell adenocarcinoma shows anticancer drug resistance. However, its detailed mechanism is unknown. We previously reported that hepatocyte nuclear factor-1beta (HNF-1beta), a transcription factor overexpressed in clear cell adenocarcinoma, might sustain chk1 protein phosphorylation to arrest the cell cycle and inhibit cell death induced by an anticancer agent. Claspin is involved in the maintenance of chk1 activation. Claspin expression was increased over time in HNF-1beta (+) cells. HNF-1beta may suppress claspin expression, sustaining chk1 protein phosphorylation. In the future, proteolytic regulation (e.g., ubiquitination) will also be investigated.
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