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

• Published in: Experimental and therapeutic medicine Vol. 19; no. 4; pp. 3017 - 3023
• Main Authors: Wu, Maosong, Tang, Yongsheng, Hu, Gang, Yang, Chunjian, Ye, Kaichuang, Liu, Xianluo
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications 01.04.2020; Spandidos Publications UK Ltd; D.A. Spandidos
• Subjects: Analysis; Apoptosis; Binding sites; Cancer; Cell cycle; Cell growth; Colorectal cancer; Endothelium; Experiments; Flow cytometry; Gene expression; Health aspects; Hemangioma; Infection; Insulin; Kinases; Lung cancer; MicroRNA; MicroRNAs; Novels; Polymerase chain reaction; Proteins; Scientific equipment industry; Tumors; United States; hemangioma; insulin-like growth factor 1 receptor; microRNA-4458; proliferation
• ISSN: 1792-0981; 1792-1015
• DOI: 10.3892/etm.2020.8546

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.