| Project/Area Number |
17K07168
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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 |
Tumor biology
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| Research Institution | Kobe University |
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Principal Investigator |
Mukai Hideyuki 神戸大学, バイオシグナル総合研究センター, 准教授 (80252758)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | protein kinase N / PKN / 血管内皮細胞 / がん転移 / PKN3 / PKN2 / PKN1 / 酵素 / がん / 動物 / シグナル伝達 / ゲノム |
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| Outline of Final Research Achievements |
Vascular endothelial cell-specific PKN2 knockout mice (mice specifically lacking PKN2 in vascular endothelial cells) were generated. The mice showed no apparent abnormalities in both reproduction and development. We examined whether metastases of mouse cancer cells are inhibited in these mice, but more examples are needed to confirm the results, which are ongoing. In addition, the angiogenic activity in these mice (the extension of new vascular branches from existing blood vessels to form a vascular network, which is known to play an important role in the development of cancer), was analyzed in vitro and in vivo, but number of cases needs to be increased to confirm the results, which are also ongoing.
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| Academic Significance and Societal Importance of the Research Achievements |
タンパク質リン酸化酵素PKN3ノックアウトマウス（PKN3を欠損したマウス）においては、がんの血行性転移が抑制されており、血管内皮細胞（血管の内表面を覆っており、腫瘍の血管への接着や浸潤に重要な働きをしている）におけるPKN3の役割に注目が集まっている。構造的に類似性の高いPKN2も、がん転移において重要な役割を持っている可能性が高いが、PKN2ノックアウトマウスは、胎児発生の段階で死んでしまうため、これまでマウス個体を用いた解析がなされていなかった。本研究の結果は、まだ確定的なものではないため公表は差し控えるが、がん転移のメカニズムの解明に知見を与えるものである。
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