3"O-methylEGCG (metylated-(3")-epigallocatechin gallate) regulated the cellular proliferation in hepatoma cell line Huh7 in vitro and in vivo.
Project/Area Number |
19590797
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Gastroenterology
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Research Institution | Kurume University |
Principal Investigator |
HASHIMOTO Osamu Kurume University, 医学部, 助教 (50289427)
|
Co-Investigator(Kenkyū-buntansha) |
UENO Takato 久留米大学, 先端癌治療研究センター, 教授 (70176618)
|
Project Period (FY) |
2007 – 2009
|
Project Status |
Completed (Fiscal Year 2009)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2008: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2007: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
Keywords | メチル化カテキン / 肝癌治療 / 肝癌の治療 / 抗酸化作用 / 抗癌剤 / 癌 / 薬理学 / 抗酸化 |
Research Abstract |
We herein report a new finding, namely, the anti-proliferate potential of MethylEGCG and attempt to clarify its mechanism of action against a Huh7 hepatoma cell line. inhibition by flow cytometry. MethylEGCG was found to induce cell proliferation at a very low concentration (5uM). The expression of pAkt was down-regulated after treatment at concentrations under 5uM. We observed the in vivo growth of a tumor graft model (5×10^6 Huh7 cells grafted in the skin of nude mice). The tumor growth of the 1mg/1kg MethylEGCG i.p and 7.5mg/kg MethylEGCG orally group showed a significant difference (after 2 weeks, vs. control ; p<0.05 and after 3 weeks, vs control ; p<0.01(n=12)). In summary, these findings suggest that MethylEGCG may be an important chemoprevention agent for the treatment of hepatoma.
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Report
(4 results)
Research Products
(7 results)