MicroRNA-223 promotes mast cell apoptosis by targeting the insulin-like growth factor 1 receptor

被引:18
作者
Gao, Haiyan [2 ]
Deng, Huan
Xu, Hong
Yang, Qianyuan
Zhou, Yao
Zhang, Jiamin
Zhao, Deyu [1 ]
Liu, Feng [1 ]
机构
[1] Nanjing Med Univ, Nanjing Childrens Hosp, Dept Resp Med, 72 Guangzhou Rd, Nanjing 210029, Jiangsu, Peoples R China
[2] Nanjing Med Univ, Huaian Peoples Hosp 1, Dept Pediat, Huaian 223300, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
microRNA-223; insulin-like growth factor-1 receptor; mast cell; apoptosis; MIR-223; PROLIFERATION; SYSTEM; OVEREXPRESSION; METASTASIS; BIOGENESIS; SUPPRESSES; DISORDERS; FAMILY;
D O I
10.3892/etm.2016.3227
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
100103 [病原生物学]; 100218 [急诊医学];
摘要
The present study aimed to examine the functional role of miR-223 in the regulation of mast cell apoptosis. Overexpressed miR-223 in mast cells transfected by Lipofectamine 2000 was used as a model, and miR-223 was found to promote mast cell apoptosis. To investigate the underlying mechanisms involved, the potential and putative target molecules of miR-223 were detected by bioinformatical analysis using predictive software, and western blotting. Insulin-like growth factor-1 receptor (IGF-1R) was found to be the functional target of miR-223 in the promotion of cell apoptosis. The downstream PI3K/protein kinase B (Akt) signaling pathway was also inhibited, and signaling was mediated by IGF-1R. Furthermore, the relative luciferase activity of the reporter containing the 3'-untranslated region (3'-UTR) of IGF-1R was significantly suppressed, while suppression of miR-223-inhibited IGF-1R protein expression was also observed. In conclusion, the results suggest that IGF-1R is the functional target for miR-223 promotion of cell apoptosis, and its downstream PI3K/Akt signaling pathway was suppressed by miR-223 through targeting of IGF-1R.
引用
收藏
页码:2171 / 2176
页数:6
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