| Project/Area Number |
26462125
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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 |
Respiratory surgery
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| Research Institution | Kyoto University |
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Principal Investigator |
MENJU Toshi 京都大学, 医学研究科, 特定病院助教 (30527081)
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| Co-Investigator(Kenkyū-buntansha) |
園部 誠 京都大学, 医学研究科, 准教授 (00432378)
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| Research Collaborator |
SABE Hisataka 北海道大学, 大学院・医学研究科・分子生物学教室, 教授
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 肺癌 / EMT / 浸潤転移 / Arf6 / GEP100 / EGFR / Grb2 / アダプター分子 |
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| Outline of Final Research Achievements |
We revealed the enhancing mechanisms of Arf6 pathway via the binding between activated EGFR and GEP100. Grb2 overexpression induces the promotion of the binding of these molecules and its downstream molecule, Arf6 invasion pathway, leading the activation of EMT and in vitro invasive activity in lung cancer cells.
Furthermore, mutant Grb2 overexpression which does not bind EGFR did not show the enhancement of Arf6 pathway. These results possibly showed the inhibition of the binding among these molecular complex is the promising targets to suppress the invasive activity in lung cancer cells
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