| Project/Area Number |
24659842
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pathobiological dentistry/Dental radiology
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|---|
| Research Institution | Ohu University |
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Principal Investigator |
|
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| Co-Investigator(Renkei-kenkyūsha) |
KIMIHARU Hirose 奥羽大学, 歯学部, 教授 (10218836)
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|---|
| Project Period (FY) |
2012-04-01 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | SPARC / AP-1 / 転写調節 / 転移 |
|---|
| Outline of Final Research Achievements |
Roles of SPARC/osteonectin on tumor growth, invasion, and metastasis, are still controversial. Because AP-1 plays common role of following gene expression, Camp, Ngp, and Saa3, whose expression was up-regulated in SPARC knockout mice, we focused on AP-1 as SPARC target to be down-regulated. AP-1 activity was upregulated by SPARC gene knockout and inhibited by introduction of SPARC expression vector having signal peptide of preprotrypsin as the secreted form. Similar results were found when we used signal peptide-deleted expression vector to induce SPARC expression as the intracellular protein. These results suggested that SPARC plays a role of AP-1 inhibition as the intracellular function.
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