The analysis and clinical applications of cellular adhesion controlmechanisms by a metastasis suppressor CD82 in an oral cancer
| Project/Area Number |
22792027
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Surgical dentistry
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| Research Institution | Matsumoto Dental University |
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Principal Investigator |
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 癌 / 遺伝子 / 細胞・組織 / シグナル伝達 / CD82 |
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| Research Abstract |
It has been proposed that the metastasis suppressor CD82 regulates biological activity by associating with cell surface receptors or proteins. We reported previously that the CD82-c-Met complex inhibits hepatocyte growth factor (HGF)-induced cancer cell migration by the inactivation of small GTP-binding proteinsof the Rho family via c-Met adapter proteins. On the other hand, β-catenin binds tothe cytoplasmic domain of E-cadherin and links E-cadherin to the actin cytoskeleton through α-actinin, forming strong intercellular junction. In addition, the function of E-cadherin is regulated by binding p120 to the cytoplasmic domain of E-cadherin.E-cadherin has been implicated not only in cell adhesion but also in the signaling of cell migration. Our results suggested that CD82 regulated the signaling ofE-cadherin-catenin-actinin-actin cell cytoskeleton and inhibited cell migration withsupporting cell adhesion.
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Report
(4 results)
Research Products
(21 results)
