| Project/Area Number |
05837003
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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 |
血管生物学
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| Research Institution | University of Tokyo |
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Principal Investigator |
OHNISHI Shin University of Tokyo, Third Department of Internal Medicine, Clinical Associate., 医学部・附属病院, 助手 (00183236)
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| Project Period (FY) |
1993 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1995: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1994: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1993: ¥600,000 (Direct Cost: ¥600,000)
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| Keywords | vascular endothelial growth factor (VEGF) / angiogenesis / hepatocellular carcinoma (HCC) |
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| Research Abstract |
Vascular endothelial growth factor (VEGF), also known as vascular permeability factor (VPF), stimulates the growth of endothelial cells in vitro and promote angiogenesis in vivo. It has been proposed to be the most potent factor of tumor associated angiogenesis. VEGF is known to interact at least two specific high affinity receptor in tyrosine kinase family, Flt-1 and KDR/Flk-1. Since hepatocellular carcinoma (HCC) is one of tumors that are caracterized by marked angiogenesis, possible involvement of vascular endothelial growth factor expression in HCC cells is suspected. In this study, I investigated whether gene and protein expression of VEGF was increased in HCC cells. Northern blot hybridization analysis revealed that HCC cells exhibited a significant elevated level of VEGF mRNA.Immunohistochemical study also showed that intense immunoreactivity against VEGF on HCC tissues. In addition, VEGF secretion by HCC cells was confirmed by Western immunoblot study. No expression of flt-1 mRNA was detected in HCC cells. These findings support for the hypothesis that VEGF may be potent factor for angiogenesis associateted with HCC and may be strongly involved in the development and progression of the tumor.
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