| Project/Area Number |
06670633
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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 |
Respiratory organ internal medicine
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| Research Institution | Nippon Medical School |
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Principal Investigator |
KUDOH Shoji Nippon Medical School, Medical Dept.Professor, 医学部, 教授 (40256912)
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| Co-Investigator(Kenkyū-buntansha) |
GEMMA Akihiko Nippon Medical School, Medical Dept.Assistant, 医学部, 助手 (20234651)
AOYAMA Akinori Nippon Medical School, Medical Dept.Lecturer, 医学部, 講師 (60089688)
SHIBUYA Masahiko Nippon Medical School, Medical Dept.Associated Profesor, 医学部, 助教授 (50142534)
竹中 圭 日本医科大学, 医学部, 助手
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1995: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1994: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | Lung Cancer / Cell Line / Metastases / Highly metastatic cell line / Nude mouse / Adhesion / Invasion / Integrin / ヒト肺癌細胞株 |
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| Research Abstract |
<ABSTRACT>Integrins are the major receptors by which cells attach to extracellular matrix and play an important role in cancer metastasis. To investigate the relation of integrins and metastasis, we established a highly metastatic human non-small cell lung cancer (NSCLC) cell line in nude mice, designated PC9/F9, by repeated intravenous injection of parent cell (PC9). In cell adhesion assay, PC9 adhered to laminin but PC9/F9 adhered more strongly. Farther more, PC9/F9 adhered type IV collagen and fibronectin. FACS scan analysis showed expression of VLA-2, VLA-3 and VLA-6 in PC9, VLA-2, VLA-3, VLA-4, VLA-5 and VLA-6 in PC9/F9. In adhesion inhibition assay, adhesion of PC9 to laminin was inhibit by anti-human alpha3 and beta1 integrin monoclonal antibody (Mo-Ab), on the other hand, adhesion of PC9/F9 to laminin was not inhibit by anti-beta1 integrin Mo-Ab and any of anti-alpha integrin Mo-Ab. Adhesion of PC9/F9 to type IV collagen was inhibited by anti-alpha2 and anti-beta1 integrin Mo-Ab. Adhesion of PC9/F9 to fibronectin was inhibit by anti-alpha5 and anti-beta1 integrin Mo-Ab. Anti-alpha4 Mo-Ab moderately inhibit adhesion of PC9/F9 to fibronectin. These data suggest that beta1 integrins enhance the ability of human NSCLC cells to metastasize by changing their expression and function.
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