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MiR-17 and miR-93 Promote Tumor Progression by Targeting p21 in Patients with Chordoma
OBJECTIVE: MicroRNAs have been implicated in the progression of various cancers. However, the role of microRNAs in chordoma remains to be further elucidated. Here, we purposed to character the role of two microRNAs, miR-17 and miR-93, and their potential mechanisms in chordoma. METHODS: The expressi...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8153071/ https://www.ncbi.nlm.nih.gov/pubmed/34054299 http://dx.doi.org/10.2147/OTT.S307138 |
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author | Dong, Wei Li, Jingwu Dong, Xiaoliu Shi, Wenjian Zhang, Yu Liu, Yongliang |
author_facet | Dong, Wei Li, Jingwu Dong, Xiaoliu Shi, Wenjian Zhang, Yu Liu, Yongliang |
author_sort | Dong, Wei |
collection | PubMed |
description | OBJECTIVE: MicroRNAs have been implicated in the progression of various cancers. However, the role of microRNAs in chordoma remains to be further elucidated. Here, we purposed to character the role of two microRNAs, miR-17 and miR-93, and their potential mechanisms in chordoma. METHODS: The expression and prognostic value of miR-17 and miR-93 were assessed by the quantitative real-time polymerase chain reaction, Kaplan–Meier survival curve, and Cox regression analysis. The effects of miR-17/93 mimics on chordoma cell proliferation, colony formation, and invasion were analyzed by CCK-8 assay, colony formation assay, and transwell assay. The downstream target of miR-17/93 was further explored via luciferase reporter assay. RESULTS: High expression of miR-17/93 was identified in chordoma tissues, and was associated with poor prognosis. Overexpression of miR-17/93 contributed to cell proliferation, colony formation, and invasion. Mechanistically, we demonstrated that miR-17/93 directly targeted p21 and decreased the expression of p21. Besides, the rescue assay further confirmed the essential role of the miR-17/93-p21 axis in chordoma. CONCLUSION: Our results revealed the potential oncogenic effect of the miR-17/93 on chordoma progression, and suggested that the miR-17/93-p21 axis served as a promising therapeutic target in chordoma. |
format | Online Article Text |
id | pubmed-8153071 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-81530712021-05-27 MiR-17 and miR-93 Promote Tumor Progression by Targeting p21 in Patients with Chordoma Dong, Wei Li, Jingwu Dong, Xiaoliu Shi, Wenjian Zhang, Yu Liu, Yongliang Onco Targets Ther Original Research OBJECTIVE: MicroRNAs have been implicated in the progression of various cancers. However, the role of microRNAs in chordoma remains to be further elucidated. Here, we purposed to character the role of two microRNAs, miR-17 and miR-93, and their potential mechanisms in chordoma. METHODS: The expression and prognostic value of miR-17 and miR-93 were assessed by the quantitative real-time polymerase chain reaction, Kaplan–Meier survival curve, and Cox regression analysis. The effects of miR-17/93 mimics on chordoma cell proliferation, colony formation, and invasion were analyzed by CCK-8 assay, colony formation assay, and transwell assay. The downstream target of miR-17/93 was further explored via luciferase reporter assay. RESULTS: High expression of miR-17/93 was identified in chordoma tissues, and was associated with poor prognosis. Overexpression of miR-17/93 contributed to cell proliferation, colony formation, and invasion. Mechanistically, we demonstrated that miR-17/93 directly targeted p21 and decreased the expression of p21. Besides, the rescue assay further confirmed the essential role of the miR-17/93-p21 axis in chordoma. CONCLUSION: Our results revealed the potential oncogenic effect of the miR-17/93 on chordoma progression, and suggested that the miR-17/93-p21 axis served as a promising therapeutic target in chordoma. Dove 2021-05-12 /pmc/articles/PMC8153071/ /pubmed/34054299 http://dx.doi.org/10.2147/OTT.S307138 Text en © 2021 Dong et al. https://creativecommons.org/licenses/by-nc/3.0/This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/ (https://creativecommons.org/licenses/by-nc/3.0/) ). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Dong, Wei Li, Jingwu Dong, Xiaoliu Shi, Wenjian Zhang, Yu Liu, Yongliang MiR-17 and miR-93 Promote Tumor Progression by Targeting p21 in Patients with Chordoma |
title | MiR-17 and miR-93 Promote Tumor Progression by Targeting p21 in Patients with Chordoma |
title_full | MiR-17 and miR-93 Promote Tumor Progression by Targeting p21 in Patients with Chordoma |
title_fullStr | MiR-17 and miR-93 Promote Tumor Progression by Targeting p21 in Patients with Chordoma |
title_full_unstemmed | MiR-17 and miR-93 Promote Tumor Progression by Targeting p21 in Patients with Chordoma |
title_short | MiR-17 and miR-93 Promote Tumor Progression by Targeting p21 in Patients with Chordoma |
title_sort | mir-17 and mir-93 promote tumor progression by targeting p21 in patients with chordoma |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8153071/ https://www.ncbi.nlm.nih.gov/pubmed/34054299 http://dx.doi.org/10.2147/OTT.S307138 |
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