| Project/Area Number |
07557199
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Osaka University |
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Principal Investigator |
NAKAMURA Toshikazu Osaka University Medical School, Professor, 医学部, 教授 (00049397)
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| Co-Investigator(Kenkyū-buntansha) |
KAWATA Sumio Osaka University Medical School, Professor, 医学部, 助教授 (90183285)
MONDEN Morito Osaka University Medical School, Professor, 医学部, 教授 (00127309)
FUNAKOSHI Hiroshi Osaka University Medical School, Assistant Professor, 医学部, 助手 (40273685)
MATSUMOTO Kunio Osaka University Medical School, Associate Professor, 医学部, 助教授 (90201780)
根本 康夫 大阪大学, 医学部, 助手 (30250088)
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| Project Period (FY) |
1995 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥6,500,000 (Direct Cost: ¥6,500,000)
Fiscal Year 1997: ¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1996: ¥4,100,000 (Direct Cost: ¥4,100,000)
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| Keywords | HGF / HGF antagonist / NK4 / c-Met / tumor / tumor-stromal interaction / invasion / metastasis / NK4 / 浸潤・転移 / 血管新生 / 浸潤・転移抑制剤 / 基底膜浸潤 / コラーゲンゲル内浸潤 / c-met / 癌細胞 / 腫瘍 / 癌浸潤・転移 / 増殖因子 / サイトカイン / レセプター |
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| Research Abstract |
Invasion and metastasis of tumor cells follows their interaction with stromal cells. Hepatocyte growth factor (HGF) is a mesenchymal- or stromal-derived mediator that affects the growth and the invasiveness of tumor cells. We prepared an antagonistic molecule, designated as HGF/NK4, from partially digested recombinant HGF.HGF/NK4 competitively inhibited the HGF binding to its receptor c-Met, and abrogated the mitogenic, motpgenic, and morphogenic actions of HGF.In addition, HGF/NK4 almost completely suppressed HGF-induced scattering and invasion of tumor cells in vitro. Furthermore, HGF/NK4 drastically inihibited growth, invasion, and metastasis of tumor cells subcutaneously implanted into nude mouse. These results suggest that there is a unique therapeutic potential for HGF/NK4 to prevent tumor invasion and metastasis.
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