| Project/Area Number |
09670242
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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 |
Experimental pathology
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| Research Institution | KURUME UNIVERSITY |
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Principal Investigator |
YANO Hirohisa Kurume University, School of Medicine, Instructor, 医学部, 講師 (40220206)
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| Co-Investigator(Kenkyū-buntansha) |
HIGAKI Koichi Kurume University, School of Medicine, Fellow, 医学部, 助手 (40289385)
OGASAWARA Sachiko Kurume University, School of Medicine, Fellow, 医学部, 助手 (40258405)
IEMURA Akihiro Kurume University, School of Medicine, Fellow, 医学部, 助手 (40212724)
KOJIRO Masamichi Kurume University, School of Medicine, Professor, 医学部, 教授 (90080580)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 1999: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1998: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1997: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Hepatocellular carcinoma / Heparin binding-growth factor-like growth factor / Epidermal growth factor family / Autocrine mechanism / Paracrine mechanism / Cell line / Immunohistochemistry / CD9 / 上皮細胞増殖因子ファミリーオートクライン / ヘパリン / 肝癌 / ジャクスタクライン |
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| Research Abstract |
HB-EGF expression was comparatively investigated in human hepatocellular carcinoma (HCC) and non-HCC tissues by using immunohistochemical technique. Both of hepatocytes and HCC cells expressed heparin binding -growth factor-like growth factor (HB-EGF) in the cytoplasm. Since HB-EGF positive rate and staining intensity tended to increase after neoplastic transformation of hepatocytes, and since the staining intensity tended to increase along with the histologic grade of HCC, a possible role of HB-EGF in the development and progression of HCC would be suggested. Sarcomatous HCCs tended to show more intensive immunostaining in the sarcomatous components than in the HCC components. HB-EGF expression was also noted in macrophages, fibroblasts, and endothelial cells in the cancerous and noncancerous sinusoids. These results suggest that HCC dells may possess a proliferation mechanism regulated by an autocrine and a paracrine mechanisms which are mediated by HB-EGF and epidermal growth factor
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(EGF) receptor. HCC cell line experiments revealed that HCC cells frequently express transforming growth factor (TGF)-α, but rarely express HB-EGF. HCC cells may possess a paracrine system regulated not only by HB-EGF, but also by TGF-α, EGF, and amphiregulin ; and an autocrine growth mechanism regulated by an unknown EGF family member and EGFR, one regulated by TGF-α and EGFR under a certain condition. Expression of CD9, which enhances a juxtacrine growth mechanism regulated by HB-EGF and EGF receptor, was observed in hepatocytes, and sinusoidal lining cells in HCC and nonHCC tissues. CD9 expression was more frequently observed in well-differentiated HCC tissues than in moderately differentiated HCC tissues. In conclusion, it was suggested that HB-EGF expression may relate with hepatocarcinogenesis and HCC progression, and that the proliferation of well differentiated HCCs may be regulated not only by a paracrine and/or an autocrine mechanisms mediated by HB-EGF, but also by a juxtacrine mechanism mediated by HB=EGF in cooperation with CD9. Less
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