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2019 Fiscal Year Final Research Report

The novel oncogenic signal with tyrosine phosphorylation induced by Ras

Research Project

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Project/Area Number 17K08641
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field General medical chemistry
Research InstitutionJichi Medical University

Principal Investigator

Ohta Satoshi  自治医科大学, 医学部, 講師 (40528428)

Project Period (FY) 2017-04-01 – 2020-03-31
KeywordsRas / 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.

Free Research Field

細胞内シグナル伝達系

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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Published: 2021-02-19  

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