miR-4458 directly targets IGF1R to inhibit cell proliferation and promote apoptosis in hemangioma

被引:7
|
作者
Wu, Maosong [1 ]
Tang, Yongsheng [1 ]
Hu, Gang [1 ]
Yang, Chunjian [1 ]
Ye, Kaichuang [2 ]
Liu, Xianluo [1 ]
机构
[1] Second Peoples Hosp Hefei, Dept Gen Surg, 246 Peace Rd, Hefei 230011, Anhui, Peoples R China
[2] Shanghai Jiao Tong Univ, Ninth Peoples Hosp, Dept Vasc Surg, Sch Med, Shanghai 230011, Peoples R China
关键词
hemangioma; microRNA-4458; insulin-like growth factor 1 receptor; proliferation; INFANTILE HEMANGIOMA; GENE-EXPRESSION; STEM-CELLS; CANCER; GROWTH; RECEPTOR; INSULIN; MICRORNA-4458; SUPPRESSES; MIGRATION;
D O I
10.3892/etm.2020.8546
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Hemangiomas (HAs) are benign neoplasms of the vasculature. MicroRNA-4458 (miR-4458) has been reported to function as a tumor suppressor in multiple malignancies, but its biological function in HAs remains unknown. In the present study, the potential role of miR-4458 in HA-derived endothelial cells (HDECs) was investigated. Firstly, reverse-transcription-quantitative PCR analysis was used to confirm the expression of miR-4458 in HDECs following transfection with miR-4458 mimics or inhibitor. Subsequently, MTT and EdU assays were performed and subsequently determined that miR-4458 overexpression significantly inhibited proliferation, and knockdown promoted cell proliferation in HDECs. Flow cytometry analysis revealed that miR-4458 overexpression induced cell cycle arrest, whereas knockdown reversed G0/G1 phase arrest and apoptosis. Furthermore, insulin-like growth factor 1 receptor (IGF1R) was identified as a target of miR-4458. IGF1R knockdown enhanced the effects of miR-4458 on cell proliferation, cell cycle G0/G1 phase arrest and apoptosis in HDECs. Taken together, the results revealed that miR-4458 targeting of IGF1R may serve as a novel therapeutic strategy for treating patients with HAs.
引用
收藏
页码:3017 / 3023
页数:7
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