Project/Area Number |
23590975
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Gastroenterology
|
Research Institution | Okayama University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
ONISHI Hideki 岡山大学, 大学院医歯薬学総合研究科, 助教 (30595468)
NAKAMURA Shinichiro 岡山大学, 岡山大学病院, 助教 (70514230)
NOUSO Kazuhiro 岡山大学, 大学院医歯薬学総合研究科, 准教授 (10314668)
YAMAMOTO Kazuhide 岡山大学, 大学院医歯薬学総合研究科, 教授 (90140491)
|
Co-Investigator(Renkei-kenkyūsha) |
MURATA Kazumoto 国立国際医療研究センタ-, 国府台病院・肝炎免疫 研究センタ-,大学院 医歯薬学総合研究科, 肝疾患先端治療室長,教授 (40345971)
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | 肝細胞癌 / Notchシグナル / 血管新生 / RUNX3 |
Research Abstract |
Runt-related transcription factor 3 (RUNX3) expression was lost or decreased in hepatocellular carcinoma (HCC) cell lines and HCC tissues. Introduction of RUNX3 cDNA suppressed Notch signal in HCC cells. The loss of RUNX3 expression induced epithelial-mesenchymal transition (EMT) in HCC. Gamma-glutamyl carboxy lase (GGCX) activity was decreased in des-gamma carboxyprothrombin (DCP)-positive HCC. DCP stimulated angiogenesis in HCC progression. DCP antibody successfully inhibited the tubular formation of the vascular endothelial cells. The decrement of GGCX activity also induced EMT in HCC.
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