| Project/Area Number |
15H04928
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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 |
Digestive surgery
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
宮下 知治 金沢大学, 附属病院, 助教 (30397210)
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| Co-Investigator(Renkei-kenkyūsha) |
OHTA Tetsuo 金沢大学, 医学系, 教授 (40194170)
SOGA Tomoyoshi 慶応義塾大学, 環境情報学部, 教授 (60338217)
SEIO Kohshi 東京工業大学, 生命理工学研究科, 准教授 (20313356)
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| Research Collaborator |
DOMOTO Takahiro 金沢大学, がん進展制御研究所, 助教 (80635540)
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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 |
¥16,640,000 (Direct Cost: ¥12,800,000、Indirect Cost: ¥3,840,000)
Fiscal Year 2017: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2015: ¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
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| Keywords | 大腸がん / 病態 / 治療 |
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| Outline of Final Research Achievements |
We explored the biological role of glycogen synthase kinase (GSK)3β in colorectal cancer (CRC) progression by focusing on the distinct metabolic profile and micro(mi)-RNA. Expression of GSK3β was increased in 70% of clinical CRC tumors, which was associated inversely with expression of tumor suppressive let-7 miRNA but not with activation of K-ras or Src oncoprotein. Metabolic analysis of GSK3β in CRC cells and tumors found that GSK3β was responsible for tumor-promoting aberrant metabolism. For translation of GSK3β-targeted therapy to cancer treatment, we also conducted preliminary studies on cancer therapeutic effects of GSK3β-inhibiting seed compounds.
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