| Project/Area Number |
14571511
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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 |
Urology
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| Research Institution | Yokohama City University |
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Principal Investigator |
KISHIDA Takeshi Yokohama City Univ.Dep.of Urology, Associate prof, 医学部附属病院, 講師 (60254166)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAIGAWA Noboru Yokohama City Univ.Dep.of Urology, Associate prof, 医学部附属病院, 講師 (00237207)
YAO Masahiro Yokohama City Univ.Dep.of Urology, Assistant prof., 医学部, 助教授 (00260787)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 2003: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2002: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | renal cell carcinom / HGF / NK4 / 増殖 / 浸潤 / 転移 |
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| Research Abstract |
In many types of cancer, HGF plays a important role in its invasion, metastasis and angiogenesis. We analyzed these role in renal cell carcinoma. In-vitro, HGF showed activation of cell growth and expression of vascular endothelial growth factor(VEGF). We also found that the tumor suppressor VHL protein negatively regulate this VEGF expression through HGF-c-MET pathway.
In order to regulate these HGF effect on renal cell carcinoma, we studied the effect of HGF antgagonist NK4, which are a part of clingle domain of HGF. In vitro, expression of NK4 by transfection method showed no effect on HGF function. To maximize the expression of NK4, we constructed Adenoviral vector and infect to the renal carcinoma cell lines. These expression of NK4 dramatically showed inhibition of cell growth activated by HGF. To see effect of NK4 in vivo, we established nude mouse subcutaneal human renal cell carcinoma tumor. We failed to show any inhibitory effect for these tumor by NK4. Further improvement of expression or way of administration will be necessary.
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