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miR-100-5p Inhibits Malignant Behavior of Chordoma Cells by Targeting IGF1R
PURPOSE: Our research aimed to illuminate the role of miR-100-5p in chordoma and potential mechanism. MATERIALS AND METHODS: We used microRNA array analysis to explore differentially expressed miRNAs in chordoma tissue and then verified by qRT-PCR. Cell proliferation and transwell assay were used to...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7293400/ https://www.ncbi.nlm.nih.gov/pubmed/32606920 http://dx.doi.org/10.2147/CMAR.S252185 |
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author | Zhang, Hongliang Yang, Kang Ren, Tingting Huang, Yi Liang, Xin Yu, Yiyang Wang, Wei Niu, Jianfang Lou, Jingbing Tang, Xiaodong Guo, Wei |
author_facet | Zhang, Hongliang Yang, Kang Ren, Tingting Huang, Yi Liang, Xin Yu, Yiyang Wang, Wei Niu, Jianfang Lou, Jingbing Tang, Xiaodong Guo, Wei |
author_sort | Zhang, Hongliang |
collection | PubMed |
description | PURPOSE: Our research aimed to illuminate the role of miR-100-5p in chordoma and potential mechanism. MATERIALS AND METHODS: We used microRNA array analysis to explore differentially expressed miRNAs in chordoma tissue and then verified by qRT-PCR. Cell proliferation and transwell assay were used to evaluate the function of miR-100-5p. Cell apoptosis was analyzed by flow cytometry, and using biological software, we predicted that the insulin-like growth factor 1 receptor (IGF1R) could be the target gene of miR-100-5p, which was then validated by dual luciferase assays and Western blot. RESULTS: miR-100-5p was downregulated in chordoma tissues. Overexpression of miR-100-5p could suppress the growth of chordoma both in vitro and in vivo, and miR-100-5p could inhibit the migration and invasion of chordoma cells partially by suppressing epithelial–mesenchymal transition (EMT). Furthermore, IGF1R was validated as the target gene of miR-100-5p and expressed in most chordoma tissues. CONCLUSION: In conclusion, our results showed that miR-100-5p was lowly expressed in chordoma and inhibited tumor malignant progression by targeting IGF1R. |
format | Online Article Text |
id | pubmed-7293400 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-72934002020-06-29 miR-100-5p Inhibits Malignant Behavior of Chordoma Cells by Targeting IGF1R Zhang, Hongliang Yang, Kang Ren, Tingting Huang, Yi Liang, Xin Yu, Yiyang Wang, Wei Niu, Jianfang Lou, Jingbing Tang, Xiaodong Guo, Wei Cancer Manag Res Original Research PURPOSE: Our research aimed to illuminate the role of miR-100-5p in chordoma and potential mechanism. MATERIALS AND METHODS: We used microRNA array analysis to explore differentially expressed miRNAs in chordoma tissue and then verified by qRT-PCR. Cell proliferation and transwell assay were used to evaluate the function of miR-100-5p. Cell apoptosis was analyzed by flow cytometry, and using biological software, we predicted that the insulin-like growth factor 1 receptor (IGF1R) could be the target gene of miR-100-5p, which was then validated by dual luciferase assays and Western blot. RESULTS: miR-100-5p was downregulated in chordoma tissues. Overexpression of miR-100-5p could suppress the growth of chordoma both in vitro and in vivo, and miR-100-5p could inhibit the migration and invasion of chordoma cells partially by suppressing epithelial–mesenchymal transition (EMT). Furthermore, IGF1R was validated as the target gene of miR-100-5p and expressed in most chordoma tissues. CONCLUSION: In conclusion, our results showed that miR-100-5p was lowly expressed in chordoma and inhibited tumor malignant progression by targeting IGF1R. Dove 2020-06-02 /pmc/articles/PMC7293400/ /pubmed/32606920 http://dx.doi.org/10.2147/CMAR.S252185 Text en © 2020 Zhang et al. http://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/). 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 Zhang, Hongliang Yang, Kang Ren, Tingting Huang, Yi Liang, Xin Yu, Yiyang Wang, Wei Niu, Jianfang Lou, Jingbing Tang, Xiaodong Guo, Wei miR-100-5p Inhibits Malignant Behavior of Chordoma Cells by Targeting IGF1R |
title | miR-100-5p Inhibits Malignant Behavior of Chordoma Cells by Targeting IGF1R |
title_full | miR-100-5p Inhibits Malignant Behavior of Chordoma Cells by Targeting IGF1R |
title_fullStr | miR-100-5p Inhibits Malignant Behavior of Chordoma Cells by Targeting IGF1R |
title_full_unstemmed | miR-100-5p Inhibits Malignant Behavior of Chordoma Cells by Targeting IGF1R |
title_short | miR-100-5p Inhibits Malignant Behavior of Chordoma Cells by Targeting IGF1R |
title_sort | mir-100-5p inhibits malignant behavior of chordoma cells by targeting igf1r |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7293400/ https://www.ncbi.nlm.nih.gov/pubmed/32606920 http://dx.doi.org/10.2147/CMAR.S252185 |
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