| Project/Area Number |
24890116
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Urology
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| Research Institution | Osaka University |
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Principal Investigator |
UEMURA Motohide 大阪大学, 医学(系)研究科(研究院), 助教 (40631015)
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| Project Period (FY) |
2012-08-31 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 腎細胞癌 / マイクロRNA / マイクロアレイ / 上皮間葉転換 |
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| Research Abstract |
To identify a therapeutic candidate target molecule for ccRCC, we analyzed the microRNA (miRNA) expression in ccRCC clinical specimens. miRNA microarray and real-time PCR analyses revealed that miR-629 expression was significantly upregulated in ccRCC compared to the adjacent non-cancerous renal tissue. Functional inhibition of miR-629 by miRNA inhibitor suppressed cell migration and invasion. MiR-629 directly targeted TRIM33, which inhibits the TGF-beta/Smad signaling pathway. MiR-629 inhibitor significantly suppressed TGF-beta-induced Smad activation by upregulating TRIM33 expression. Moreover, miR-629 inhibition attenuated the effect of TGF-beta on the expression of epithelial-mesenchymal transition (EMT)-related factors in ccRCC cell lines. In clinical ccRCC specimens, downregulation of TRIM33 was observed with the association of both pathological stages and grades. Our findings indicate that miR-629 is a potent regulator of the TGF-beta/Smad signaling pathway via TRIM33 in ccRCC.
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