| Project/Area Number |
17K07150
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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 | Hokkaido University |
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Principal Investigator |
Haga Hisashi 北海道大学, 先端生命科学研究院, 教授 (00292045)
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| Co-Investigator(Kenkyū-buntansha) |
小林 純子 (仁尾純子) 北海道大学, 医学研究院, 講師 (70447043)
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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: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 細胞・組織 / がん細胞 / 集団運動 / 接触追従 / 電子顕微鏡 / 集団浸潤 |
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| Outline of Final Research Achievements |
Collective invasion, in which cancer cells invade as a cell population, is associated with the metastatic potential and prognosis of cancer patients. The collectiveness of cancer cells is a necessary attribute for collective invasion. However, the mechanism that causes cancer cells to form collectiveness is not currently well known. To investigate this mechanism, we focused on contact following, which is the phenomenon that instigates the movement of neighboring cells in the same direction via intercellular adhesion. In this study, we show that the intercellular expression of extracellular matrix proteins (type-XVII collagen and laminin-332) and integrin-β1 promotes contact following in collective invasion. Our findings suggest that integrin-extracellular matrix interaction in the intercellular site could be a new therapeutic target for treating cancer with collective invasion potential.
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| Academic Significance and Societal Importance of the Research Achievements |
がん細胞の浸潤に関する研究は，これまで主に単一の細胞を対象に行われてきた．一方，実際の生体内では，がん細胞は組織内を集団で浸潤することが知られている．このことを集団浸潤とよぶ．本研究は，がん細胞の接触追従という性質に着目し，集団浸潤の機序を解明することを目的に，接着タンパク質インテグリンβ1に着目して，接触追従を担う分子およびシグナル経路の同定を目指した．その結果，本研究によって接触追従の機序の一端が明らかとなった．今後は，接触追従に関与するタンパク質を薬剤投与などで失活させるなどがん細胞の浸潤を抑えるための新たな創薬ターゲット，および治療法の開発につながることが期待される．
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