| Project/Area Number |
15K14387
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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 |
Tumor biology
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| Research Institution | Miyagi Prefectural Hospital Organization Miyagi Cancer Center |
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Principal Investigator |
ITO Shigemi 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)
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| Co-Investigator(Kenkyū-buntansha) |
田沼 延公 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)
佐藤 郁郎 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), ティッシュバンクセンター, センター長 (50225918)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 肺がん / Pkm / NAD代謝 / グルコース代謝 / がん細胞の特性 |
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| Outline of Final Research Achievements |
In this study, we investigated whether cellular metabolism can be explored as novel therapeutic target of small cell lung cancer (SCLC). We found that neuroendocrine tumors, a subset of lung cancer, exhibit substantial expression of Pkm1. Functional analyses revealed that Pkm1, but not Pkm2, can fully support proliferation of the SCLC cell-lines, suggesting their dependence on Pkm1. We also found that an inhibitor on NAD salvage suppresses growth of PKM1-expressing cancer cells, suggesting a therapeutic strategy for PKM1-positive tumors such as SCLC
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