| Project/Area Number |
23659643
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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(Kenkyū-buntansha) |
KAWAKAMI Kazuyuki 金沢大学, がん進展制御研究所, 准教授 (00293358)
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| Co-Investigator(Renkei-kenkyūsha) |
SOGA Tomoyoshi 慶應義塾大学, 環境情報学部, 教授 (60338217)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 消化器がん / エネルギー代謝 / 標的治療 / GSK3β |
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| Research Abstract |
Recently we discovered novel pathological roles for glycogen synthase kinase-3β (GSK3β) in promoting cancer cell survival and proliferation via the modulation of cell cycle, tumor suppressor and cell immortality pathways. This has led us to propose GSK3β as a potential target for cancer treatment. A primary role for GSK3β is the control of glycogen synthase activity that switches glycogenesis and glycolysis, the two major pathways of glucose metabolism. In this research, we investigated whether GSK3β influences the aberrant glucose metabolism in gastrointestinal cancer cells. Using innovative metabolomic technology, we found a distinctive metabolic trait in cancer cells that suggests inhibition of GSK3β attenuates glycolysis (Warburg effect) and restores mitochondrial glucose oxidation.This trait could be an important molecular basis for cancer treatment targeting aberrant GSK3β.
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