| Project/Area Number |
24510277
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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 |
Medical genome science
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| Research Institution | Hiroshima University |
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Principal Investigator |
HIRANO Tetsuo 広島大学, 総合科学研究科, 助教 (50228805)
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| Co-Investigator(Renkei-kenkyūsha) |
HARADA Hironori 順天堂大学, 医学部, 准教授 (10314775)
HARADA Yuka 順天堂大学, 医学部, 助教 (50379848)
ISHIDA Atsuhiko 広島大学, 総合科学研究科, 教授 (90212886)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
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| Keywords | 機能性非コードRNA / 骨髄性白血病 / 増殖制御 / 血清飢餓 / 遺伝子ノックダウン / shRNA / 受容体型チロシンキナーゼ / KIT / ノックダウン / チロシンキナーゼ型受容体 / 非コード性RNA / 疾患関連遺伝子 / 染色体外因子 |
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| Outline of Final Research Achievements |
A long noncoding RNA, CCDC26, which is reportedly the most common gene whose copy number is altered in pediatric acute myeloid leukemia cells. We identified some transcripts abundant in myeloid leukemia cells within the CCDC26 genetic locus, and the concentration of these transcripts in the nuclei of the cells. Knock down of CCDC26 resulted in the prolonged survival period of the cells in the culture medium without serum. The expression of KIT, a well known oncogene functioning as a receptor tyrosine kinase, was significantly enhanced in the CCDC26-knock down cells, suggesting that this gene controls proliferation of the myeloid leukemia cells through KIT expression. These result might give an impact to the therapy strategy for myeloid leukemia with mutated CCDC26 genes.
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