| Project/Area Number |
21591754
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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 |
Digestive surgery
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
MAEHARA Yoshihiko 九州大学, 医学研究院, 教授 (80165662)
TAKETOMI Akinobu 九州大学, 大学病院, 講師 (70363364)
IKEGAMI Toru 九州大学, 大学病院, 助教 (80432938)
副島 雄二 九州大学, 大学病院, 助教 (30325526)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | マイクロRNA / 肝細胞癌 / 肝移植 / マイクロアレイ / リアルタイムPCR / リアルタイムPCR法 / C型肝炎 / マイクロRNAマイクロアレイ |
|---|
| Research Abstract |
The expression of microRNA(miR) on hepatocellular carcinoma(HCC) was comprehensively examined by miR microarray. miR was extracted from 3 HCC cases who underwent liver transplantation. We detected miR-18a which showed high expression in cancerous lesion, and miR-199a-3p which existed in non cancerous liver tissue.
The quantitative expression analysis of miR was done using a real-time PCR method. The miR samples were collected from 70 HCC cases which underwent liver transplantation. The result showed the level of miR-18a was significantly high in cancerous lesion(T/N=1. 8), and miR-199a was significantly deteriorated in cancerous lesion(T/N=0. 31). The higher miR-18a and lower miR-199a were significantly correlated with higher serum AFP and DCP, and larger tumor diameter. Furthermore, those cases showed significantly worse recurrence-free survival rate after surgery.
The molecular function was analyzed in vivo using cultured HCC cells. Target genes of miR-18a, 199awere detected using online database. We examined THFAIP3 ; target gene of miR-18a and HIF1R and cdc42 ; those of miR-199a. The expression of these target genes were significantly inhibited by transfection of the miRs in HCC cells. Our study indicated that miR-18a and miR-199a had important role on the progression of HCC.
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