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2018 Fiscal Year Final Research Report

Exploring stress-responsive molecules involved in cell competition

Planned Research

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Project AreaCell competition: a mechanism for survival of the fittest in the multi-cellular community
Project/Area Number 26114009
Research Category

Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)

Allocation TypeSingle-year Grants
Review Section Biological Sciences
Research InstitutionThe University of Tokyo

Principal Investigator

Ichijo Hidenori  東京大学, 大学院薬学系研究科(薬学部), 教授 (00242206)

Project Period (FY) 2014-07-10 – 2019-03-31
Keywords細胞競合 / Scribble / トランスクリプトーム解析 / 液性因子 / ASK1
Outline of Final Research Achievements

In this study, using Scribble knock down model, we scrutinized the molecular mechanism of cell competition, which is considered to be involved in early cancer elimination and ontogenesis. First, we established a high-throughput quantitation system of cell competition, using high content image analyzer. Then, we performed a transcriptome analysis focusing on the difference between normal and transformed cells and a candidate approach focusing on MAP kinase pathway. From these results, we found that a humoral factor that is expressed through ASK1-p38 pathway is required for cell competition induced by Scribble depletion.

Free Research Field

分子生物学

Academic Significance and Societal Importance of the Research Achievements

本研究では、全自動ハイコンテントイメージアナライザーを用いて、精密な細胞競合の測定系を構築した。またそれを利用してこれまで分子メカニズムが不明であった哺乳類細胞における細胞競合において、ASK1-p38経路というシグナル伝達経路が形質転換細胞であるScribble欠損細胞内で活性化し、特定の液性因子の発現を誘導すること、またその液性因子が正常細胞に感知されて細胞競合が引き起こされることを明らかにした。これらの知見は、細胞競合現象の理解を深めるとともに、細胞競合の関わる初期のがんの排除などを制御する薬剤の具体的なターゲットを提示した点で意義があると考えられる。

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Published: 2020-03-30  

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