Elucidating the mechanism of cancer cell evolution via cell-cell interaction
| Project/Area Number |
17K19594
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology and related fields
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| Research Institution | Kyoto University |
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Principal Investigator |
Enomoto Masato 京都大学, 生命科学研究科, 助教 (00596174)
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| Project Period (FY) |
2017-06-30 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2019: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2018: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | がん / 細胞間相互作用 / Ras / Src / 細胞融合 / 細胞肥大化 / シグナル伝達 / 細胞間コミュニケーション |
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| Outline of Final Research Achievements |
Although cancer tissues are composed of heterogeneous tumor cell populations, it is still poorly understood how distinct tumor cells contribute to cancer progression. In this situation, I found that two MDCK cells activating oncogenic Ras and Src cause cell fusion when they coexisted. This result suggests that distinct tumor cells drives cancer cell evolution via cell-cell interaction. In this project, I aimed to dissect the mechanism by which Ras and Src cells developed into newly generated tumor cells via cell fusion. I found that Src cells cause cellular hypertrophy of Ras cells via cell-cell interaction. Interestingly, hypertrophic Ras cells have capability of cell fusion and behave as the leader cell in collective cell migration. Furthermore, I found that Src cells secrete glutamate in extracellular space to cause cellular hypertrophy of Ras cells. These findings suggest that Src-activating cells provide additive function to Ras-activating cells for tumor progression.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究の成果は、異なる２種類の腫瘍細胞が細胞間相互作用を介して新しい機能を獲得することを哺乳類培養細胞系において明らかにした。このことは、がん組織において近接する２つの腫瘍細胞同士がその機能・役割を制御し合っている可能性を示唆している。将来的には、生体内において細胞間相互作用を介した腫瘍細胞の機能制御の普遍原理を解明しその制御方法を確立することで、新たながん治療戦略や抗がん剤開発の基盤になることが期待される。
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Report
(4 results)
Research Products
(11 results)
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[Journal Article] Drosophila As a Cancer Model2018
Author(s)
Masato Enomoto, Carmen Siow, Tatsushi Igaki
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Journal Title
Advances in Experimental Medicine and Biology
Volume: 1076
Pages: 173-194
DOI
ISBN
9789811305283, 9789811305290
Related Report
Peer Reviewed
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