| Project/Area Number |
25870947
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Biological pharmacy
Tumor biology
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| Research Institution | Tokyo University of Science |
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Principal Investigator |
Nagano Makoto 東京理科大学, 基礎工学部, 研究員 (50572715)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | がん増殖 / がん悪性化 / 細胞-ECM間接着 / 三次元培養 / 細胞生物学 / がん浸潤・転移 / 浸潤性がん細胞 / 三次元増殖 |
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| Outline of Final Research Achievements |
In this study, I focus on the regulatory mechanism to adapt tumor cells to survive in the three-dimensional cell－extracellular matrix adhesion environment. First, I established the MKN7-derived cell, which has acquired growth actvity in the 3D environment. To identify the key proteins in 3D growth of the cells, I compared the levels of the expression or the phosphorylation of the multiple proteins including signal-, oncology- or stress-related molecules, to the parental MKN7 cells. I elucidated that the phosphorylation of STAT3 is promoted and the down-stream target Bcl-x, which has a suppressive role in the apoptosis, is increased. Furthermore, several proteases such as MMP-9, Cathepsin L are increased, whereas some types of protease inhibitors including HAI-I/2, Maspin are decreased. These results suggest that the apoptosis suppression via STAT-3 signaling and the some types of protease activity are crucial for the tumor adaptation to the three-dimensional adhesion environment.
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