Disruption of Eph receptor signaling in cancer cells
| Project/Area Number |
18K06215
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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 44010:Cell biology-related
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| Research Institution | Kyoto University |
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Principal Investigator |
Katoh Hironori 京都大学, 生命科学研究科, 准教授 (50303847)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | がん / 受容体 / シグナル伝達 / 細胞運動 / エフリン / グルコース / 神経膠芽腫 / 浮遊培養 |
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| Outline of Final Research Achievements |
The ephrin receptor (Eph) plays various roles in the developmental process, such as nerve axon guidance and vascular guidance, by binding to the ligand ephrin in normal tissues. On the other hand, it has been reported that the Eph receptor is highly expressed in cancer cells, suggesting that it is involved in cancer malignant transformation. In this study, it was newly found that 1) EphA3 acts in a ligand-independent manner to promote the formation of glioblastoma cell aggregates under suspension culture conditions, 2) EphA2 promotes glioblastoma cell survival under glucose-limited conditions in a ligand-independent manner, and 3) overexpression of EphA3 promotes cell motility.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究は、がん細胞においてのみ特に活性化されているEph受容体シグナルに焦点を絞り、そのシグナル伝達に関わる分子を網羅的に解析していくことで、がんの悪性化を担う新たなシグナル伝達の一端を解明することをめざすとともに、がん細胞の悪性度の違いを分子レベルで明らかにしていくことを目的とする。本研究による成果は、副作用の少ない抗がん剤やがんの悪性度を示す新たな指標の創出に寄与する可能性が考えられる。
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Report
(4 results)
Research Products
(19 results)
