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miR-19b-1 通过阻断内皮细胞的细胞周期进程来抑制血管生成。

MiR-19b-1 inhibits angiogenesis by blocking cell cycle progression of endothelial cells.

机构信息

Pharmaceutical Research Center, School of Chemistry & Chemical Engineering, Southeast University, Nanjing 211189, China.

出版信息

Biochem Biophys Res Commun. 2012 Jan 13;417(2):771-6. doi: 10.1016/j.bbrc.2011.12.032. Epub 2011 Dec 16.

DOI:10.1016/j.bbrc.2011.12.032
PMID:22197821
Abstract

MicroRNAs are endogenously expressed small, non-coding RNAs that modulate biological processes by recognizing specific gene transcripts, leading to translational repression or degradation. Previous work showed that the miR-17-92 cluster is highly expressed in human endothelial cells that participate in angiogenesis. In this study we showed that miR-19b-1, a component of this cluster, controls the intrinsic angiogenic activity of human umbilical vein endothelial cells (HUVECs) in vitro. In silico and in vitro analyses have suggested that miR-19b-1 targets mRNA corresponding to the pro-angiogenic protein, FGFR2, and blocks the cell cycle from the S phase to the G(2)/M phase transition by controlling the expression of cyclin D1. Thus, miR-19b-1 may serve as a valuable therapeutic agent in the context of tumor angiogenesis.

摘要

微 RNA 是内源性表达的小非编码 RNA,通过识别特定的基因转录本来调节生物过程,导致翻译抑制或降解。先前的工作表明,miR-17-92 簇在参与血管生成的人内皮细胞中高度表达。在这项研究中,我们表明该簇的组成部分 miR-19b-1 控制体外人脐静脉内皮细胞(HUVEC)的内在血管生成活性。计算机分析和体外分析表明,miR-19b-1 靶向对应于促血管生成蛋白 FGFR2 的 mRNA,并通过控制细胞周期蛋白 D1 的表达将细胞周期从 S 期阻滞到 G2/M 期过渡。因此,miR-19b-1 可能在肿瘤血管生成的背景下作为一种有价值的治疗剂。

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