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Function of Ecotropic Viral Integration Site 1 (EVI1) gene in neural precurser cells and human glioma cells

Research Project

Project/Area Number 25462275
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Neurosurgery
Research InstitutionUniversity of Miyazaki

Principal Investigator

Kiyotaka Yokogami  宮崎大学, 医学部, 講師 (40284856)

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)
Project Period (FY) 2013-04-01 – 2016-03-31
Project Status Completed (Fiscal Year 2015)
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)
KeywordsEVI1 / EGFR / neural precurser cell / glioma / glioma initiating cell / NOTCH / GIC / integrin / laminin / Notch / VEGF
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.

Report

(3 results)
  • 2015 Annual Research Report   Final Research Report ( PDF )
  • 2013 Research-status Report
  • Research Products

    (3 results)

All 2015 2013

All Presentation (3 results)

  • [Presentation] 脳腫瘍における転写因子EVI1 の機能解明2015

    • Author(s)
      横上聖貴
    • Organizer
      第33回日本脳腫瘍学会
    • Place of Presentation
      京都市
    • Year and Date
      2015-12-06
    • Related Report
      2015 Annual Research Report
  • [Presentation] 脳腫瘍における転写因子EVI1 の機能解明2015

    • Author(s)
      横上聖貴
    • Organizer
      第16回日本分子脳神経外科学会
    • Place of Presentation
      浜松市
    • Year and Date
      2015-08-28
    • Related Report
      2015 Annual Research Report
  • [Presentation] マウス神経幹細胞とグリオーマ幹細胞におけるEvi1の機能解析2013

    • Author(s)
      横上聖貴、水口惣平、水口麻子、 山崎浩司、竹島秀雄
    • Organizer
      第31回日本脳腫瘍学会学術集会
    • Place of Presentation
      フェニックスシーガイアリゾート(宮崎県宮崎市)
    • Related Report
      2013 Research-status Report

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Published: 2014-07-25   Modified: 2019-07-29  

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