| Project/Area Number |
24590124
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | Yokohama College of Pharmacy (2014)
Showa University (2012-2013) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
ISHII Masakazu 昭和大学, 薬学部, 准教授 (30307061)
NEGORO Takaharu 昭和大学, 薬学部, 講師 (70218270)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ＴＲＰＭ２ / 固形がん / カルシウムイオン / サイトカイン / 血管新生 / マクロファージ / TRPM2 チャネル / 腫瘍 / 活性酸素 / TRPM2 / 悪性腫瘍 / 腫瘍関連マクロファージ / ケモカイン |
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| Outline of Final Research Achievements |
This study examined whether TRPM2 channels contribute to tumor growth. The tumor growth by injection s.c. with lung cancer cells was suppressed in TRPM2 knockout (KO) mice. Angiogenesis, number of macrophages and angiogenesis-stimulating cytokines, all of which are stimulating factors for tumor growth, were increased in the tumor of TRPM2 KO mice. Moreover, TRPM2 expression was observed in macrophages, and the channels were activated by H2O2. These findings suggest that TRPM2 channels in macrophages contribute to tumor growth, and may be a candidate as target molecule for new anti-cancer drug.
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