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miR-222-3p promotes osteosarcoma cell migration and invasion through targeting TIMP3
BACKGROUND: Abnormal expression of miRNAs has been reported in osteosarcoma (OS), and miR-222-3p levels have been found to be increased in the serum of OS patients. However, the exact role of miR-222-3p in OS remains unclear. In the present study, we aimed to identify the molecular mechanism underly...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove Medical Press
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6284535/ https://www.ncbi.nlm.nih.gov/pubmed/30584323 http://dx.doi.org/10.2147/OTT.S175745 |
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author | Guo, Jianping Liu, Quanxiang Li, Zengxin Guo, Haifeng Bai, Changshuang Wang, Fajia |
author_facet | Guo, Jianping Liu, Quanxiang Li, Zengxin Guo, Haifeng Bai, Changshuang Wang, Fajia |
author_sort | Guo, Jianping |
collection | PubMed |
description | BACKGROUND: Abnormal expression of miRNAs has been reported in osteosarcoma (OS), and miR-222-3p levels have been found to be increased in the serum of OS patients. However, the exact role of miR-222-3p in OS remains unclear. In the present study, we aimed to identify the molecular mechanism underlying the role of miR-222-3p in the development of OS. METHODS: We examined the expression level of miR-222-3p in OS tissues and OS cells using reverse-transcription quantitative PCR (RT-qPCR) analysis. MTT, colony formation, and transwell invasion assays were used to analyze the effects of miR-222-3p on the proliferation and invasion ability of OS cells. Luciferase reporter gene assays were used to confirm the target gene of miR-222-3p in OS cells. Tumor xenografts were then used to investigate the role of miR-222-3p in OS growth in vivo. RESULTS: The data of the present study demonstrated that miR-222-3p levels were increased in OS tissues and OS cells. Downregulation of miR-222-3p significantly inhibited the proliferation, migration, and invasion of OS cells in vitro. Further analysis revealed that tissue inhibitors of metalloproteinases 3 (TIMP3) is one of the functional target genes of miR-222-3p, and inhibition of TIMP3 efficiently rescues the blocking of cell proliferation and invasion mediated by miR-222-3p inhibitor in OS cells. CONCLUSION: Our findings constitute evidence that miR-222-3p promotes OS cell proliferation and invasion through targeting TIMP3 mRNA and provide novel insight into the mechanism underlying the development of OS. |
format | Online Article Text |
id | pubmed-6284535 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-62845352018-12-24 miR-222-3p promotes osteosarcoma cell migration and invasion through targeting TIMP3 Guo, Jianping Liu, Quanxiang Li, Zengxin Guo, Haifeng Bai, Changshuang Wang, Fajia Onco Targets Ther Original Research BACKGROUND: Abnormal expression of miRNAs has been reported in osteosarcoma (OS), and miR-222-3p levels have been found to be increased in the serum of OS patients. However, the exact role of miR-222-3p in OS remains unclear. In the present study, we aimed to identify the molecular mechanism underlying the role of miR-222-3p in the development of OS. METHODS: We examined the expression level of miR-222-3p in OS tissues and OS cells using reverse-transcription quantitative PCR (RT-qPCR) analysis. MTT, colony formation, and transwell invasion assays were used to analyze the effects of miR-222-3p on the proliferation and invasion ability of OS cells. Luciferase reporter gene assays were used to confirm the target gene of miR-222-3p in OS cells. Tumor xenografts were then used to investigate the role of miR-222-3p in OS growth in vivo. RESULTS: The data of the present study demonstrated that miR-222-3p levels were increased in OS tissues and OS cells. Downregulation of miR-222-3p significantly inhibited the proliferation, migration, and invasion of OS cells in vitro. Further analysis revealed that tissue inhibitors of metalloproteinases 3 (TIMP3) is one of the functional target genes of miR-222-3p, and inhibition of TIMP3 efficiently rescues the blocking of cell proliferation and invasion mediated by miR-222-3p inhibitor in OS cells. CONCLUSION: Our findings constitute evidence that miR-222-3p promotes OS cell proliferation and invasion through targeting TIMP3 mRNA and provide novel insight into the mechanism underlying the development of OS. Dove Medical Press 2018-12-03 /pmc/articles/PMC6284535/ /pubmed/30584323 http://dx.doi.org/10.2147/OTT.S175745 Text en © 2018 Guo et al. 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. |
spellingShingle | Original Research Guo, Jianping Liu, Quanxiang Li, Zengxin Guo, Haifeng Bai, Changshuang Wang, Fajia miR-222-3p promotes osteosarcoma cell migration and invasion through targeting TIMP3 |
title | miR-222-3p promotes osteosarcoma cell migration and invasion through targeting TIMP3 |
title_full | miR-222-3p promotes osteosarcoma cell migration and invasion through targeting TIMP3 |
title_fullStr | miR-222-3p promotes osteosarcoma cell migration and invasion through targeting TIMP3 |
title_full_unstemmed | miR-222-3p promotes osteosarcoma cell migration and invasion through targeting TIMP3 |
title_short | miR-222-3p promotes osteosarcoma cell migration and invasion through targeting TIMP3 |
title_sort | mir-222-3p promotes osteosarcoma cell migration and invasion through targeting timp3 |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6284535/ https://www.ncbi.nlm.nih.gov/pubmed/30584323 http://dx.doi.org/10.2147/OTT.S175745 |
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