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微小RNA-31的条件性敲除促进结肠炎相关癌症的发展。

Conditional knockout of microRNA-31 promotes the development of colitis associated cancer.

作者信息

Liu Zhaoyuan, Bai Jing, Zhang Lingyun, Lou Fangzhou, Ke Fang, Cai Wei, Wang Honglin

机构信息

Shanghai Institute of Immunology, Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.

Shanghai Institute of Immunology, Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China; Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.

出版信息

Biochem Biophys Res Commun. 2017 Aug 12;490(1):62-68. doi: 10.1016/j.bbrc.2017.06.012. Epub 2017 Jun 6.

DOI:10.1016/j.bbrc.2017.06.012
PMID:28600172
Abstract

MicroRNA-31 (miR-31) is an evolutionarily conserved microRNA, and its biological function in colorectal cancer and other cancers is controversial. In this study, we identified the host gene of mouse miR-31 and found that miR-31 was over-expressed in both human colorectal cancer and mouse colon cancer models. We here developed a miR-31 conditional knockout mouse model that allows for colon epithelium specific deletion of miR-31 to investigate its functionality in colon cancer development. We demonstrated that mice with miR-31 conditional deletion resulted in more severe colitis-associated cancer than wild-type, and we further identified Wdr5 as an important target of miR-31.

摘要

微小RNA-31(miR-31)是一种进化上保守的微小RNA,其在结直肠癌和其他癌症中的生物学功能存在争议。在本研究中,我们鉴定了小鼠miR-31的宿主基因,并发现miR-31在人类结直肠癌和小鼠结肠癌模型中均过度表达。我们在此构建了一种miR-31条件性敲除小鼠模型,该模型允许在结肠上皮中特异性缺失miR-31,以研究其在结肠癌发生中的功能。我们证明,与野生型相比,miR-31条件性缺失的小鼠导致更严重的结肠炎相关癌症,并且我们进一步确定Wdr5是miR-31的一个重要靶标。

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