| Project/Area Number |
25670572
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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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(Renkei-kenkyūsha) |
SUGIYAMA Naoyuki 慶應義塾大学, 政策・メディア研究科, 特任講師 (50545704)
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| Research Collaborator |
DOMOTO Takahiro
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 大腸がん / 蛋白質リン酸化 / GSK3β |
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| Outline of Final Research Achievements |
The phosphoproteomic approach explored the putative biological mechanism by which glycogen synthase kinase (GSK)3β promotes colon cancer progression. Inhibition of GSK3β significantly modified the level of phosphorylation in a number of proteins in colon cancer cells. Integration of phosphoproteome and metabolome analysis for these proteins phosphorylated by GSK3β identified the enzyme A, a rate-limiting enzyme in glucose metabolism, which was preferentially phosphorylated by GSK3β in cancer cells. The results suggest that GSK3β promotes cancer progression by induction of aberrant glucose metabolism via phosphorylation-dependent inactivation of the enzyme A. In all, this study demonstrates that cancer treatment targeting GSK3β depends on modulation of cancer-specific profile of protein phosphorylation.
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