2013 Fiscal Year Final Research Report
microRNA-125b inhibits tumor vascular formation through translational suppression of VE-cadherin
Project/Area Number |
23701054
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Tumor biology
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Research Institution | Osaka University |
Principal Investigator |
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Project Period (FY) |
2011 – 2013
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Keywords | マイクロRNA / 血管新生 / 細胞接着 / 癌治療 / 核酸医薬 |
Research Abstract |
MicroRNAs (miRNAs) are endogenously expressed small non-coding RNAs that function as negative regulators of gene expression. Posttranscriptional regulation by miRNAs is important for many aspects of development and disease. Sveral miRNAs are highly expressed in endothelial cells. Whereas the specific functions of miRNAs for tumor angiogenesis are less clear. Here, we identified miRNAs that were enriched in endothelial cells derived from LLC tumor. We found that miR-125b regulated the expression of endothelial cell adherent protein VE-cadherin. Additionally, overexpression of miR-125b in endothelial cells resulted in inhibition of proliferation, tube formation and migration activity. Furthermore, in vivo transfection of mir-125b in subcutaneous implanted LLC tumor, inhibited neo vascular formation and suppressed tumor growth. These findings illustrate that mir-125b act as negative regulator of tumor angiogenesis and providing a new target for modulating vascular formation and function.
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[Journal Article] Critical role of Trib1 in differentiation of tissue-resident M2-like macrophages2013
Author(s)
Satoh T, Kidoya H, Naito H, Yamamoto M, Takemura N, Nakagawa K, Yoshioka Y, Morii E, Takakura N, Takeuchi O, Akira S
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Journal Title
Nature
Volume: Mar 28;495(7442)
Pages: 524-8
DOI
Peer Reviewed
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