2019 Fiscal Year Final Research Report
The novel oncogenic signal with tyrosine phosphorylation induced by Ras
Project/Area Number |
17K08641
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General medical chemistry
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Research Institution | Jichi Medical University |
Principal Investigator |
Ohta Satoshi 自治医科大学, 医学部, 講師 (40528428)
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Project Period (FY) |
2017-04-01 – 2020-03-31
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Keywords | Ras / Mer / IL-33 / がんの悪性化 / がん |
Outline of Final Research Achievements |
In this research project, we attempted to clarify the role of Mer tyrosine kinase (Mer) in the novel oncogenic signal, Ras/IL-33 pathway. In the previous study, we concluded that Ras accelerates the expression of Mer in depending on IL-33. We found that IL-33 and Mer were required for Ras-induced cellular migration. Ras signal promoted the phosphorylation of Mer and the kinase activity of Mer was necessary for Ras-induced cellular migration. Taken together, it is suggested that Ras/IL-33 pathway contributes the cancer malignant progression via Mer tyrosine kinase.
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Free Research Field |
細胞内シグナル伝達系
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Academic Significance and Societal Importance of the Research Achievements |
Ras遺伝子の変異によるRasシグナルの異常な活性化は、多くのがんの原因となることが知られており、特に難治性がんの一つである膵がんでは約90%の患者でRas遺伝子の変異が見つかっている。Rasの下流シグナルに関してもMAPキナーゼをはじめとして多くの知見が集積している一方で、MAPキナーゼ経路を標的とした抗がん剤治療には、耐性を示す患者も多く存在する。本研究によって新規Rasシグナルの構成因子とその機能が明らかなることは、今後の抗がん剤開発において重要な基盤となると期待される。
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