| Project/Area Number |
22592103
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pathobiological dentistry/Dental radiology
|
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| Research Institution | The Nippon Dental University |
|---|
Principal Investigator |
IMAI Kazushi 日本歯科大学, 生命歯学部, 教授 (10328859)
|
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| Co-Investigator(Kenkyū-buntansha) |
CHIBA Tadashige 日本歯科大学, 生命歯学部, 准教授 (60350138)
MORIKAWA Masako 日本歯科大学, 生命歯学部, 准教授 (80095265)
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| Project Period (FY) |
2010 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2012: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2011: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2010: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
|
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| Keywords | 口腔癌 / MALT1 |
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| Research Abstract |
The present study examined a role of mucosa-associated lymphoid tissue 1 (MALT1), whose expression is inactivated in oral carcinomas with worse prognosis, in oral carcinoma cells and its involvement in phenotypic alteration of the cells by the microarray and proteomic analyses. MALT1 down-regulated expression of genes in the TGF-ss and EGF pathways, alternated keratin species involved in aggressive feature of carcinoma cells, and suppressed proliferation and migration of the cells. Furthermore, E-cadherin-mediated carcinoma cell-cell adhesion machinery, which was also strongly down-regulated by MALT1, was rapidly obstructed with progression of oral carcinomas.
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