| Project/Area Number |
23791150
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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 |
Pediatrics
|
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| Research Institution | Yamagata University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 抗腫瘍免疫 / 樹状細胞療法 / STAT3 / エピジェネティックス / HDAC / エピジェネティクス |
|---|
| Research Abstract |
Epigenetic regulation via STAT3 and HDACs in bone marrow derived dendritic cells potentially enhances anti-tumor effect. In this study, we demonstrated the STAT3-HDAC7 axis had a key role and induces tumor elimination in tumor bearing mouse model. The STAT3 deficient dendritic cells revealed enhanced expression of MHC class II, CD80, 86, 40 and IL-12, IL-6, IL-10 expression. In this model, STAT3 bound HDAC7 promoter and probably regulates cytokine expression. Thus, HDACs uniquely regulate tumor growth with STAT3. And the therapeutic application of HDACi should be elucidated in the future.
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