| Project/Area Number |
23659700
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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 |
Cerebral neurosurgery
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| Research Institution | Miyagi Cancer Center Research Institute |
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Principal Investigator |
KATAKURA Ryuuichi 地方独立行政法人宮城県立病院機構宮城県立がんセンター(研究所), がん薬物療法研究部, 特任研究員 (10442675)
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| Co-Investigator(Kenkyū-buntansha) |
ITO Sigemi 地方独立行政法人宮城県立病院機構宮城県立がんセンター(研究所), がん薬物療法研究部, 特任研究員 (80600006)
TANUMA Nobuhiro 地方独立行政法人宮城県立病院機構宮城県立がんセンター(研究所), がん薬物療法研究部, 主任研究員 (40333645)
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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: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 代謝 / 解糖系 / ワールブルグ効果 / PKM / グリオーマ |
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| Research Abstract |
Pre-mRNA splicing of gene encoding pyruvate kinase M (PKM), a glycolytic enzyme, was dys-regulated, so that expression of PKM isoforms switches from normal- to tumor-type in human glioma. This aberrant splicing was associated with increased levels of a splicing modulator. Experiments using cell-lines showed that suppression of the splicing regulator results in partial restoration of expression of a normal-type PKM isoform. Additionally, we developed mice model in which the isozyme-conversion of PKM is disabled.
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