| Project/Area Number |
15K09478
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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 |
Hematology
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| Research Institution | Kumamoto University |
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Principal Investigator |
MATSUI HIROTAKA 熊本大学, 大学院生命科学研究部(医), 教授 (60379849)
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| Research Collaborator |
SHINRIKI Satoru 熊本大学, 大学院生命科学研究部, 准教授
NAGAMACHI Akiko 広島大学, 原爆放射線医科学研究所, 助教
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | ゲノム編集 / 急性骨髄性白血病 / 骨髄異形成症候群 / DDX41 / DDX41遺伝子 / DNAメチル化 / 造血器腫瘍 / エピゲノム |
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| Outline of Final Research Achievements |
To elucidate the pathogenesis of hematopoietic tumors caused by gene mutations or deletions, we applied genome editing for leukemia cell lines and cord blood-derived CD34 positive hematopoietic progenitor cells. In this study, we targeted the DDX41, where germ line as well as somatic mutations are observed at a certain rate, for gene editing. We previously revealed that DDX41 protein plays a role in the processing of pre-ribosomal RNA, however, its physiological function and the role of its mutant for leukemogenesis has not been elucidated so far.
We found that a leukemia cell line that does not express DDX41, established using CRISPR/CAS9 system, showed growth inhibition as compared with control cells. We assume this was caused by the inhibition of ribosome biogenesis, and further studies using these cells are underway.
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