2020 Fiscal Year Final Research Report
Toward understanding the mechanism of the relationship between CD133 and autophagy
| Project/Area Number |
18K07223
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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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| Review Section |
Basic Section 50010:Tumor biology-related
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| Research Institution | 地方独立行政法人佐賀県医療センター好生館(ライフサイエンス研究所) |
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Principal Investigator |
IZUMI HIDEKI 地方独立行政法人佐賀県医療センター好生館(ライフサイエンス研究所), ライフサイエンス研究所, 部長 (10397987)
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| Co-Investigator(Kenkyū-buntansha) |
李 元元 千葉県がんセンター(研究所), その他部局等, その他 (00392259)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Keywords | CD133 / がん幹細胞 / オートファジー / 中心体 / 非対称分裂 |
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| Outline of Final Research Achievements |
CD133 is a transmembrane protein and has been recently reported to be localized in cytoplasms. However, the mechanism of action and function of cytoplasmic CD133 remains unknown. In this study, CD133 interacts with HDAC6 and is transported via the dynein-based transport system to the pericentrosome region. Subsequently, endosomal CD133 inhibit the initiation of autophagy, resulting in suppression of cell differentiation such as neurite outgrowth and primary cilia formation. Furthermore, endosome CD133 itself was found to be degraded by p62 / SQSTM1-mediated selective autophagy. Finally, endosomal CD133 cooperated with nuclear beta-catenin to induce asymmetric cell division.
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| Free Research Field |
分子腫瘍学
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| Academic Significance and Societal Importance of the Research Achievements |
私たちの研究成果は、中心体近傍型のCD133エンドソームが癌細胞の未分化状態を維持する上で重要な役割を果たすことを示し、また、中心体近傍型のCD133エンドソームは、核のベータ・カテニンと協力して、オートファジー活性に基づく非対称分裂を誘導することを示し、がん幹細胞マーカーの新しい機能を明らかにした。
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