| Project/Area Number |
25463109
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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 |
Surgical dentistry
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| Research Institution | Hiroshima University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
HAYASHIDO YASUTAKA 広島大学, 病院(歯), 講師 (70243251)
OKAMOTO TETSUJI 広島大学, 医歯薬保健学研究院, 教授 (00169153)
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| Research Collaborator |
USUI EMIKO
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | HBｐ１７ / 口腔癌 / 血管新生 / FGF結合タンパク / HBp17/FGFBP |
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| Outline of Final Research Achievements |
We tested the hypothesis that HBp17/FGFBP-1 expression was regulated by NF-кB by manipulating this particular binding site, and then studied the possibility to inhibit the activation of FGF-2 in OSCC cells by repressing the expression of HBp17/FGFBP-1 using VD3.HBp17/FGFBP-1 mRNA and protein level were significantly down-regulated by VD3.The level of IκBα, which is known as an NFκB regulator was up-regulated. As a result of a luciferase reporter assay, promoter activity of HBp17/FGFBP-1 was 30% suppressed by the VD3 treatment. Although VD3 did not show to have direct effect on FGF-2 expression, it has been revealed by ELISA that the level in the medium conditioned by the cells treated with VD3 significantly decreased. The data from quantitative RT-PCR, western blotting, and ELISA clearly showed that down-regulation of HBp17/FGFBP-1 resulted in inhibition of the FGF-2 release from the extracellular matrix.
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