1993 Fiscal Year Final Research Report Summary
Inhavition mechanism of oral cancer invasion
| Project/Area Number |
04671222
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
外科・放射線系歯学
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| Research Institution | Osaka university |
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Principal Investigator |
SHIRASUNA Kanemitsu Osaka University Faculty of Dentistry, 1st Department of Oral and Mxillofacial Surgery, Associate Professor, 歯学部, 助教授 (30093420)
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| Project Period (FY) |
1992 – 1993
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| Keywords | Salivary gland tumor / Invaion / Extracellular matrix / Protease / Protease inhibitor / Matrix degradation / Motility / Integrin |
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| Research Abstract |
In order to study invasion mechanism of oral cancer, I mainly used ACCS line derived from adenoid cystic carcinoma (ADCC).
The findings obtained from the present projedt are :
1. ACCS cells produce uPA, MMP-2 and MMP-9, and can degrade condiderable amount of ECM elaborated by normal mesenchymal cells, through mainly uPA-plasmin cascade.
ACCS cells vigorously produce extracellular matorix (ECM), including fibronectin, laminin, and type IV collagen. the ACCS-ECM is resistant to degradation by its own proteolytic enzymes because of the presence of abundant PAI-1 in the ECM.
ACCS-ECM promotes haptotactic motility of ACCS cells.
Chemotactic response of ACCS cells to laminin and type cancer cells suggesting relation to a special proclivity of ADCC cells to invade nerve and endothelial sheaths.
EGF causes enhancement of cell migration and uPA production.
Dezamethasone causes inhibition of cell migration and uPA production but enhancement of PAI-1
ECM-induced migration is inhibited by monoclonal antibodies against integrins.
A factor purified from conditioned medium with human fibroblasts, which is heaprin-unbinded protein, enhances chemotactic migration of cancer cells.
Another one from fibroblasts enhances protease production by cancer cells.
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