| Project/Area Number |
08457166
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Osaka University |
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Principal Investigator |
KAWATA Sumio Osaka University, Medical School, Associate Professor, 医学部, 助教授 (90183285)
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| Co-Investigator(Kenkyū-buntansha) |
KISO Shinichi Osaka University, Hospital, Fellow, 医学部・附属病院, 医員
MATSUDA Yukihiko Osaka University, Medical School, Assistant, 医学部, 助手 (90283770)
TAMURA Shinji Osaka University, Medical School, Assistant, 医学部, 助手 (30243223)
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| Project Period (FY) |
1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 1996: ¥3,700,000 (Direct Cost: ¥3,700,000)
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| Keywords | hepatocellular cacinoma / TGF-beta receptor / cell growth / 細胞増殖 |
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| Research Abstract |
We have studied molecular mechanisms of human hepatocarcinogenesis from the view of the point that hepatocytes have an autonomous proliferative potential due to a loss of the responsiveness to a potent negative growth regulator, TGF-beta. Previously, we found poor response of human hepatoma-derived cell lines to TGF-beta.
Hepatocellular carcinoma (HCC) occurs in the liver with HBV-or HCV-related cirrhosis. We introduced HBx gene into mink lung epithelial cell, a cell line which is very sensitive to TGF-beta. The responsiveness to TGF-beta in the transfectants was much poorer than that in the parent cells. In addition, the reduced responsiveness seemed to result from a decrease in expression of TGF-beta receptors. The hepatocytes could escape from the negative growth regulation by TGF-beta due to expression of HBx gene during chronic HBV infection.
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