| Project/Area Number |
15590619
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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 |
Gastroenterology
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| Research Institution | Gunma University |
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Principal Investigator |
TAKAGI Hitoshi Gunma University, Department of Medicine and Molecular Science, Graduate School of Medicine, Associate Professor, 大学院・医学系研究科, 助教授 (20251093)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2004: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2003: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | hepatocellular carcinoma / EGF receptor / PPAR-ganma / ZD1839 / pioglitazone / rosiglitazone / 肝臓 / EGF recepter / Apoptosis |
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| Research Abstract |
Hepatocellular carcinoma is one of the most intractable cancers in the world. Recent progress of molecular targeting enables the specific growth inhibition of cancer cells by the receptor agonist or antagonist. EGF-receptor is abundant in liver cancer cell but the effect of EGF receptor antagonist on hepatoma has not been proved to be effective. On the other hand, we have clarified the three-hepatocellular carcinoma cell lines including PLC/PRF/5, Huh7 and HepG2 were induced apoptosis by PPAR ganma agonist, rosiglitazone and pioglitazone. Furthermore anticancer drugs epirubicine more enhanced the apoptosis than 5FU and CDDP. Then we tested the collaborative effect of EGF-receptor antagonist on the PPAR agonist. As a result, pioglitazone enhanced the effect of ZD1839. The expression of EGF-R assayed by real time PCR was decreased in HepG2 compared with the other two lines but it was not correlated the effect of ZD1839.
Further study using nude mice and TGFalpha transgenic mice bearing liver cancer are on schedule.
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