| Project/Area Number |
25870717
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
Pathological medical chemistry
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| Research Institution | Keio University |
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Principal Investigator |
TAMADA Mayumi 慶應義塾大学, 医学部, 特任助教 (80528133)
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| Research Collaborator |
SAYA Hideyuki 慶應義塾大学, 医学部, 教授 (80264282)
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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 |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 癌 / 糖代謝 / pyruvate kinase M2 / 代謝変動 / 既存薬 / 解糖系 / グルコース代謝 / 好気性解糖 / ミトコンドリア呼吸 |
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| Outline of Final Research Achievements |
Recently, PKM2 has been reported to be one of the most important factors to maintain glycolic phenotype which is the unique character of cancer. Thus, the possibility of PKM2 activator as an anti-cancerous drug has attracted attention. We investigated to discover PKM2 activator, which induce the metabolic shift from aerobic glycolysis to mitochondrial respiration mainly used by normal cells, out of existing drugs.
We examined whether there was the drug which inhibits glucose consumption, lactate production, and tyrosine phosphorylation of PKM2 out of existing drugs, based on our idea that PKM2 activator may be included in the drugs which inhibit glucose consumption.We have already found some candidate drugs, and advance examination such as measurement of PKM2 enzyme activity, metabolic shift, and anti-cancerous effect.
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