| Project/Area Number |
25893113
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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 |
Biological pharmacy
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| Research Institution | Osaka University |
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Principal Investigator |
JINGUSHI Kentaro 大阪大学, 薬学研究科(研究院), 研究員 (80707571)
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| Research Collaborator |
TSUJIKAWA Kazutake
NONOMURA Norio
UEMURA Motohide
FUJITA Kazutoshi
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| Project Period (FY) |
2013-08-30 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | miR-629 / TGF-bシグナル伝達経路 / ccRCC / EMT / TGF-β/Smadシグナル伝達経路 |
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| Outline of Final Research Achievements |
This is the first study showing significant upregulation of miR-629 in ccRCC specimens by quantitative real-time PCR analysis. We demonstrate that miR-629 downregulates TRIM33 expression, leading to the association of Smad2/3 and Smad4 and then to the promotion of the TGFb/Smad signaling pathway. Moreover, we clarify that TRIM33 is significantly downregulated in ccRCC tissues compared with that in the adjacent noncancerous renal tissues, which seems to correlate with pathologic stages and grades. Our findings show that miR-629 is a potent regulator of the TGFb/Smad signaling pathway and accelerates ccRCC cell motility and invasion.
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