| Project/Area Number |
16K21646
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
Hematology
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| Research Institution | National Cancer Center Japan |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | Glis2 / Ring1A/B / 白血病幹細胞 / AML / 白血病 / ポリコーム |
|---|
| Outline of Final Research Achievements |
Glis2 is a zinc finger transcription factor, and its expression is repressed by polycomb group proteins Ring1A/B in leukemia cells. To clarify the significance of repression of Glis2 by Ring1A/B in leukemia cells, we determined the effect of Glis2 deletion on the phenotype of Ring1A/B-deleted leukemia cells. Deletion of Ring1A/B induced differentiation and elimination of leukemic stem cell in MOZ-TIF2 AML mice. On the other hand, additional deletion of Glis2 prevented differentiation of leukemic stem cells induced by Ring1A/B deficiency. These results suggest that Glis2 is an important target of Ring1A/B involved in maintenance of undifferentiated state of leukemic stem cells.
Moreover, we identified spiB as a crucial target of Glis2 in the regulation of leukemic cell differentiation.
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