2023 Fiscal Year Final Research Report
Investigation of cell-cell adhesion structures and signaling pathways causing collective invasion in cancer cells
Project/Area Number |
21K07142
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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 |
Review Section |
Basic Section 50010:Tumor biology-related
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Research Institution | Hokkaido University |
Principal Investigator |
Haga Hisashi 北海道大学, 先端生命科学研究院, 教授 (00292045)
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Co-Investigator(Kenkyū-buntansha) |
小林 純子 (仁尾純子) 長崎大学, 高度感染症研究センター, 准教授 (70447043)
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Project Period (FY) |
2021-04-01 – 2024-03-31
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Keywords | 細胞・組織 / がん細胞 / 集団浸潤 / 細胞間接着構造 / 電子顕微鏡 |
Outline of Final Research Achievements |
Many types of cancer cells invade the stroma collectively while maintaining intercellular adhesion. This phenomenon is referred to as collective invasion. This study aimed to elucidate the mechanism of collective invasion and identify the associated signaling pathways by focusing on the intercellular adhesion structures. In this study, we have shown that collective invasion in human squamous epithelial carcinoma cells (A431 cells) is triggered by the accumulation of Interferon-beta between cells, leading to the activation of STAT1. Furthermore, we discovered that the secreted protein CCL5 induces collective invasion, and an inhibitor of CCR5, the receptor for CCL5, successfully suppresses collective invasion.
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Free Research Field |
腫瘍生物学
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Academic Significance and Societal Importance of the Research Achievements |
がん細胞に関する研究は,これまで主に単一の細胞を用いて実験が行われてきた.しかし,実際の生体内では,がん細胞はお互いに接着した状態で浸潤することが知られている.そこで,本研究では,Ⅰ型コラーゲンゲルを用いて,がん細胞が集団で浸潤する様子を観察する実験系を構築し,さらに細胞間の接着構造に着目することで,集団浸潤の分子メカニズムに迫った.本研究の成果として,インターフェロンβなど複数のタンパク質が集団浸潤に関わることを明らかにした.これら結果は,将来的にがん細胞の浸潤を抑える創薬研究および治療法の開発へと展開することが期待できる.
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