miR‑4458 directly targets IGF1R to inhibit cell proliferation and promote apoptosis in hemangioma
Autor: | Xianluo Liu, Gang Hu, Maosong Wu, Yongsheng Tang, Chunjian Yang, Kaichuang Ye |
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Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Cancer Research Cell cycle checkpoint proliferation medicine.medical_treatment Cell 03 medical and health sciences 0302 clinical medicine Immunology and Microbiology (miscellaneous) medicine Insulin-like growth factor 1 receptor Gene knockdown Cell growth Chemistry Growth factor Articles General Medicine Cell cycle hemangioma 030104 developmental biology medicine.anatomical_structure insulin-like growth factor 1 receptor Apoptosis 030220 oncology & carcinogenesis Cancer research microRNA-4458 |
Zdroj: | Experimental and Therapeutic Medicine |
ISSN: | 1792-1015 1792-0981 |
DOI: | 10.3892/etm.2020.8546 |
Popis: | 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. |
Databáze: | OpenAIRE |
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