| Project/Area Number |
25462275
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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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| Research Field |
Neurosurgery
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| Research Institution | University of Miyazaki |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
Yamashita Shinji 宮崎大学, 医学部, 助教 (40468046)
MIZUGUCHI Asako 宮崎大学, 医学部, 助教 (00647472)
MIZUGUCHI Souhei 宮崎大学, 医学部, 助教 (50398103)
TAKESHIMA Hideo 宮崎大学, 医学部, 教授 (70244134)
MORISHITA Kazuhiro 宮崎大学, 医学部, 教授 (80260321)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | EVI1 / EGFR / neural precurser cell / glioma / glioma initiating cell / NOTCH / GIC / integrin / laminin / Notch / VEGF |
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| Outline of Final Research Achievements |
Ecotropic viral integration site 1 (EVI1) gene encodes a transcription factor, containing ten zinc finger motifs. Abnormal expression of EVI1 is found in 5-10% of patients with acute myeloid leukemia, and is also associated with poor outcome of patients with glioblastoma and ependymoma. EVI1 maintains the self-renewal capacity of hematopoietic stem cell. However, it is unclear how EVI1 acts in normal brain development and in brain tumor development.
In this study we found that EVI1 (-/-) neural precursor cells (NPCs) differentiated to neuron and glial cells earlier than wild type. Notch signals were altered in EVI1(-/-) NPCs. In glioblastoma, we found that EVI1 transcriptionally regulates the EGFR gene expression. Because EGF signaling in glioma initiating cells (GICs) is necessary to maintain the stemness, EVI1 has a pivotal role to maintain the GICs through EGFR gene expression.
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