| Project/Area Number |
15592113
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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 |
Surgical dentistry
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
YOSHIOKA Yukio Hiroshima University, Graduate School of Biomedical Sciences, Assistant Professor, 大学院・医歯薬学総合研究科, 助手 (20335665)
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| Co-Investigator(Kenkyū-buntansha) |
TANI Ryouji Hiroshima University, Hospital, Assistant Professor, 病院・助手 (10291486)
TANAKA Yoshiharu Hiroshima University, Hospital, Assistant Professor, 病院・助手 (50304431)
OKAMOTO Tetsuji Hiroshima University, Graduate School of Biomedical Sciences, Professor, 大学院・医歯薬学総合研究科, 教授 (00169153)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2003: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | β-Catenin / oral squamous cell carcinoma / Wnt signaling pathway / plasmin / plasminogen / E-cadherin / α2-anti-plasmin / metastasis / invasion / gene therapy |
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| Research Abstract |
The participation of plasminogen activator/plasmin system in the expression and function of E-cadherin was examined in oral squamous cell carcinoma (SCC) cells. Treatment of SCC cells with plasminogen reduced the Ca2+ -dependent cell aggregation. SCC cells expressed E-cadherin at the cell aggregation. SCC cells expressed E-cadherin at the membrane, and released a small amount of soluble E-cadherin at 80 kDa in the culture medium. Addition of plasminogen to SCC cells led to a decrease in the amount of E-cadherin of the cell membrane and the enhancement of the shedding of E-cadherin Ectodomein. Plasmin, directly cleaved E-cadherin of SCC cells and enhanced the motility of SCC cells. these results suggested that plasminogen activator/plasmin system might directly mediate the proteolytic processing of E-cadherin in oral SCC cells and that might facilitate the progression of oral SCC by downreguration of E-cadherin-mediated cell-cell adhesion.
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