Decay of RNA binding protein involved in oral oncogenesis
| Project/Area Number |
24592824
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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 |
Pathobiological dentistry/Dental radiology
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| Research Institution | Hokkaido University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
HIGASHINO Fumihiro 北海道大学, 大学院歯学研究科, 准教授 (50301891)
SHINNDOU Masanobu 北海道大学, 大学院歯学研究科, 教授 (20162802)
KITAMURA Tetsuya 北海道大学, 大学院歯学研究科, 助教 (00451451)
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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 |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 口腔外科一般 / ARE-mRNA / pp32ｒｌ / HuR / caspase3 / 口腔がん / pp32r1 / pp32 / 核害輸送 / 安定化 / 核外輸送 |
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| Outline of Final Research Achievements |
In this study, we examined how pp32r1 controls the decay of HuR to contribute tumorigenesis. In the cancer cells expressing high level pp32r1, the expression of HuR was up-regulated. pp32r1 inhibited the activity of caspase3, which is required for the HuR degradation. pp32r1 bound to HuR stronger than that of pp32. These findings indicate that pp32r1 plays the important role for transforming cells by inhibit caspase activity.
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Report
(4 results)
Research Products
(17 results)
