| Project/Area Number |
20590392
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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 | Asahikawa Medical College |
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Principal Investigator |
OGAWA Katsuhiro Asahikawa Medical College, 医学部, 名誉教授 (50045514)
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| Co-Investigator(Kenkyū-buntansha) |
柳沼 裕二 旭川医科大学, 医学部, 准教授 (90250571)
玉川 進 旭川医科大学, 医学部, 助教 (70188415)
山本 雅大 旭川医科大学, 医学部, 助教 (30431399)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2010: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2009: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2008: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
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| Keywords | IRES / 肝癌 / 蛋白合成 / 蛋白翻訳 / 肝発癌 / マウス / ラバマイシン / HIF-1 / ラパマイシン |
|---|
| Research Abstract |
Although protein translation is activated by the PI3K-Akt-mTOR pathway in mouse hepatocarcinogenesis, rapamycin, a mTOR inhibitor, shows the limited antitumor effect on hepatocellular carcinomas and no effect on hepatic adenomas despite the fact that the cap-dependent protein translation is inhibited by rapamycin. Under the condition with rapamycin treatment, HIF-1α can continue to be expressed by the internal ribosomal entry site (IRES) mechanism. Furthermore, the mechanism of tumor necrosis induced by rapamycin was not due to the direct action against hepatocellular carcinoma cells but rather due to the angiotoxic effect of rapamycin against the vasculature of hepatocellular carcinomas.
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