miR-873 suppresses H9C2 cardiomyocyte proliferation by targeting GLI1

MicroRNAs (miRNAs) are a class of endogenous, non-coding small RNAs that regulate the expression of target genes. Previous studies have suggested that miRNAs are key regulators in cardiovascular systems. This study investigated the role of miR-873 in H9C2 cardiomyocytes by targeting glioma-associate...

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Veröffentlicht in:Gene 2017-08, Vol.626, p.426-432
Hauptverfasser: Zhang, Jing-Shu, Zhao, Yue, Lv, Yuan, Liu, Pei-Yan, Ruan, Jun-Xia, Sun, Yue-Ling, Gong, Tian-xing, Wan, Nan, Qiu, Guang-Rong
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Sprache:eng
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Zusammenfassung:MicroRNAs (miRNAs) are a class of endogenous, non-coding small RNAs that regulate the expression of target genes. Previous studies have suggested that miRNAs are key regulators in cardiovascular systems. This study investigated the role of miR-873 in H9C2 cardiomyocytes by targeting glioma-associated oncogene 1 (GLI1). miR-873 was significantly up-regulated in serum samples from congenital heart disease (CHD) patients compared with those from normal individuals. Furthermore, miR-873 over-expression suppressed H9C2 proliferation and induced cell cycle arrest. Bioinformatic algorithms revealed a predicted target site for miR-873 in the 3′-untranslated region (3′UTR) of GLI1, which was verified using a dual-luciferase reporter assay. qPCR and western blot analysis also showed that miR-873 negatively regulated GLI1 mRNA and protein expression in H9C2 cells. Conversely, GLI1 over-expression partially reversed the growth-inhibitory effect of miR-873. To summarize, our data suggest that miR-873 is a novel miRNA that regulates H9C2 cell proliferation via targeting GLI1, and miR-873 may serve as a new potential biomarker diagnosis in CHD in the future. •miR-873 expression is upregulated in CHD serum samples.•miR-873 suppresses cardiomyocyte proliferation and induced cell cycle arrest.•GLI1 is a direct target of miR-873 and miR-873 suppresses GLI1 expression by direct binding to the 3′-UTR.•GLI1 overexpression reverses the effects of miR-873.
ISSN:0378-1119
1879-0038
DOI:10.1016/j.gene.2017.05.062