| Project/Area Number |
20592205
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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 | Oita University |
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Principal Investigator |
KAWANO Kenji 大分大学, 医学部, 教授 (50214664)
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| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2008: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 口腔扁平上皮癌 / 浸潤 / 転移 / 接着分子 / アノイキス / anoikis / 口腔扁平上癌 |
|---|
| Research Abstract |
Multicellular aggregates of MOK205, an oral squamous carcinoma cell line, transformed to monolayer colonies on laminin 5 and type 1 collagen substrates, and then showed cell dispersion only on laminin 5. This phenomenon was triggered by the increased motility and disruption of E-cadherin-mediated intercellular adhesion via the activation of integrin receptor by laminin 5. When PP1, a specific inhibitor of the Src family, was added to the cell scattering model of MOK205, cell dispersion was almost completely blocked, suggesting that Src was involved in the interaction between integrin and cadherin. In addition, fluorescence microscopic observation revealed that phospho-tyrosine 215-Src and phospho-tyrosine 529-Src were localized along the cell membrane of the intercellular adhesion of MOK205 immediately before cells started dispersion on laminin 5. Taken together, these results suggested that Src could be a target of the invasion/metastasis inhibition therapy against oral squamous cell carcinomas.
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