| Project/Area Number |
24592005
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SHIRABE Ken 九州大学, 医学(系)研究科(研究院), 准教授 (70264025)
MAEHARA Yoshihiko 九州大学, 医学(系)研究科(研究院), 教授 (80165662)
EGUCHI Hidetoshi 九州大学, 大学病院, 講師 (90527756)
IGUCHI Tomohiro 九州大学, 大学病院, 助教 (30598959)
AKIYOSHI Sayuri 九州大学, 大学病院, 助教 (50567360)
SUDO Tomoya 九州大学, 大学病院, 助教 (50309803)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 肝細胞癌 / 血管新生 / アペリン / F13A / CD34 / アペリンーAPJ / 血管新生阻害 / 分子標的治療 |
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| Outline of Final Research Achievements |
The aim of this study was to clarify the role of the apelin-APJ system which regulates angiogenesis in tumor progression of hepatocellular carcinoma (HCC). Expressions of angiogenic factors and vascular markers were investigated in specimens from 90 HCC patients. A subcutaneous HCC tumor mouse model was treated with the APJ antagonist, F13A, and tumor growth and vascular development were assessed. APJ expression was observed in arteriole-smooth muscle. Higher amounts of APJ+-arteriole and apelin were detected in tumors (p<0.001 for both). APJ+-arteriole and apelin expression were more commonly observed in moderately- and poorly-differentiated than in well-differentiated HCC (p=0.003). HCC with irregular dilated arteries expressed higher levels of apelin (p=0.012). Tumor growth was inhibited by treatment with F13A (p<0.001), and arterioles were decreased in the treated group (p=0.047), in vivo. Apelin-APJ is overexpressed, and works as a signal for arteriogenesis in HCC.
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