miR-200a Modulate HUVECs Viability and Migration

被引：23

作者：

Li, Yi-Xuan

Liu, Da-Quan

Zheng, Chen

Zheng, Shu-Qi

Liu, Min

Li, Xin

Tang, Hua ^{[1
,2
]}

机构：

[1] Tianjin Med Univ, Tianjin Life Sci Res Ctr, Tianjin 300070, Peoples R China

[2] Tianjin Med Univ, Basic Med Sch, Tianjin 300070, Peoples R China

来源：

IUBMB LIFE | 2011年 / 63卷 / 07期

基金：

中国国家自然科学基金;

关键词：

miR-200a; angiogenesis; HUVECs; thrombospondin-1; cell viability; cell migration; ENDOTHELIAL-CELLS; GENE-EXPRESSION; ANGIOGENESIS; MICRORNAS; DICER; APOPTOSIS;

D O I：

10.1002/iub.486

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

The posttranscriptional regulation of miRNAs is important for organism development. To investigate the role of miRNAs in angiogenesis, we performed a loss-of-function screening assay in human umbilical vein endothelial cells (HUVECs) and found that knockdown of 7 miRNAs (miR-95a, miR-126, miR-129, miR-137, miR-139, miR-200a, and miR-335) significantly suppressed cell viability. As miR-200a was highly expressed in HUVECs, blocking endogenous miR-200a using 2'-OMe antisense oligonucleotide (ASOs) resulted in a decrease of cell viability and migration. Bioinformatics analysis indicates the 3' untranslated region (UTR) of thrombospondin-1 (THBS1) has a putative binding site for miR-200a. MiR-200a can directly bind to THBS1 3'UTR and negatively regulate THBS1 expression. The identification of endothelial cells (ECs) related miRNA and its target gene may gain new insight into the mechanism of angiogenesis. (C) 2011 IUBMB IUBMB Life, 63(7): 553-559, 2011

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页码：553 / 559

页数：7

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