Analysis of highly expressed miR-629 in clear cell renal cell carcinoma

2014 Fiscal Year Final Research Report

• Project/Area Number: 25893113
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Single-year Grants
• Research Field: Biological pharmacy
• Research Institution: Osaka University
• Principal Investigator: JINGUSHI Kentaro 大阪大学, 薬学研究科(研究院), 研究員 (80707571)
• Research Collaborator: TSUJIKAWA Kazutake ; NONOMURA Norio ; UEMURA Motohide ; FUJITA Kazutoshi
• Project Period (FY): 2013-08-30 – 2015-03-31
• Keywords: miR-629 / TGF-bシグナル伝達経路 / ccRCC

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.

Free Research Field

分子腫瘍学