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miR-4458 directly targets IGF1R to inhibit cell proliferation and promote apoptosis in hemangioma
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 (...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7086214/ https://www.ncbi.nlm.nih.gov/pubmed/32256788 http://dx.doi.org/10.3892/etm.2020.8546 |
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author | Wu, Maosong Tang, Yongsheng Hu, Gang Yang, Chunjian Ye, Kaichuang Liu, Xianluo |
author_facet | Wu, Maosong Tang, Yongsheng Hu, Gang Yang, Chunjian Ye, Kaichuang Liu, Xianluo |
author_sort | Wu, Maosong |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-7086214 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-70862142020-04-02 miR-4458 directly targets IGF1R to inhibit cell proliferation and promote apoptosis in hemangioma Wu, Maosong Tang, Yongsheng Hu, Gang Yang, Chunjian Ye, Kaichuang Liu, Xianluo Exp Ther Med Articles 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. D.A. Spandidos 2020-04 2020-02-25 /pmc/articles/PMC7086214/ /pubmed/32256788 http://dx.doi.org/10.3892/etm.2020.8546 Text en Copyright: © Wu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Wu, Maosong Tang, Yongsheng Hu, Gang Yang, Chunjian Ye, Kaichuang Liu, Xianluo miR-4458 directly targets IGF1R to inhibit cell proliferation and promote apoptosis in hemangioma |
title | miR-4458 directly targets IGF1R to inhibit cell proliferation and promote apoptosis in hemangioma |
title_full | miR-4458 directly targets IGF1R to inhibit cell proliferation and promote apoptosis in hemangioma |
title_fullStr | miR-4458 directly targets IGF1R to inhibit cell proliferation and promote apoptosis in hemangioma |
title_full_unstemmed | miR-4458 directly targets IGF1R to inhibit cell proliferation and promote apoptosis in hemangioma |
title_short | miR-4458 directly targets IGF1R to inhibit cell proliferation and promote apoptosis in hemangioma |
title_sort | mir-4458 directly targets igf1r to inhibit cell proliferation and promote apoptosis in hemangioma |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7086214/ https://www.ncbi.nlm.nih.gov/pubmed/32256788 http://dx.doi.org/10.3892/etm.2020.8546 |
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