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 (...

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Published inExperimental 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
LanguageEnglish
Published Greece Spandidos Publications 01.04.2020
Spandidos Publications UK Ltd
D.A. Spandidos
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Abstract 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.
AbstractList 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.
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. Key words: hemangioma, microRNA-4458, insulin-like growth factor 1 receptor, proliferation
Audience Academic
Author Ye, Kaichuang
Hu, Gang
Liu, Xianluo
Yang, Chunjian
Wu, Maosong
Tang, Yongsheng
AuthorAffiliation 1 Department of General Surgery, The Second People's Hospital of Hefei, Hefei, Anhui 230011, P.R. China
2 Department of Vascular Surgery, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 230011, P.R. China
AuthorAffiliation_xml – name: 2 Department of Vascular Surgery, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 230011, P.R. China
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Keywords hemangioma
insulin-like growth factor 1 receptor
microRNA-4458
proliferation
Language English
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This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, 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.
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Snippet Hemangiomas (HAs) are benign neoplasms of the vasculature. MicroRNA-4458 (miR-4458) has been reported to function as a tumor suppressor in multiple...
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StartPage 3017
SubjectTerms 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
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Title miR-4458 directly targets IGF1R to inhibit cell proliferation and promote apoptosis in hemangioma
URI https://www.ncbi.nlm.nih.gov/pubmed/32256788
https://www.proquest.com/docview/2384423002/abstract/
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https://pubmed.ncbi.nlm.nih.gov/PMC7086214
Volume 19
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