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Long non-coding RNA MEG3 suppresses survival, migration, and invasion of cervical cancer
BACKGROUND: Long non-coding RNAs nowadays emerge as important biomarkers or potential therapeutic targets discussed in human cancers. Among them, maternally expressed gene 3 (MEG3) is known to be decreased in a variety of malignancies, and this affects tumor cellular proliferation, migration, and in...
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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/PMC6109651/ https://www.ncbi.nlm.nih.gov/pubmed/30174437 http://dx.doi.org/10.2147/OTT.S167053 |
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author | Chen, Xiuhui Qu, Junying |
author_facet | Chen, Xiuhui Qu, Junying |
author_sort | Chen, Xiuhui |
collection | PubMed |
description | BACKGROUND: Long non-coding RNAs nowadays emerge as important biomarkers or potential therapeutic targets discussed in human cancers. Among them, maternally expressed gene 3 (MEG3) is known to be decreased in a variety of malignancies, and this affects tumor cellular proliferation, migration, and invasion. MATERIALS AND METHODS: Quantitative real-time PCR was performed to detect the expression of MEG3 in normal cervical epithelium, cervical intraepithelial neoplasia, and cervical squamous cell carcinoma tissues. Gain-of-function and loss-of-function studies were carried out to determine the effect of MEG3 on cell survival, migration, and invasion, which was evaluated by CCK-8 assay, wound healing assay, and transwell assays. mRNA and protein expression of Rac1 were finally determined by quantitative real-time PCR and immunoblotting, respectively. In addition, rescue experiments were performed by overexpression of Rac1. RESULTS: The expression of MEG3 was downregulated in cervical intraepithelial neoplasia and squamous cell carcinoma tissues. Forced expression of MEG3 led to reduced abilities of cell survival. Overexpression of MEG3 also inhibited cell migration and invasion in vitro. Cell proliferation marker and EMT markers were changed consistently with the phenotype. In addition, Rac1 was inhibited by MEG3 overexpression at both transcriptional and translational levels. Also, Rac1 could rescue the phenotype caused by long non-coding RNA MEG3. And, it negatively correlated with MEG3 expression in cervical cancer (CC) tissues and cell lines. CONCLUSION: Our findings revealed that MEG3 could negatively regulate CC cell survival, migration, and invasion. It might serve as an important target for CC treatment. |
format | Online Article Text |
id | pubmed-6109651 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-61096512018-08-31 Long non-coding RNA MEG3 suppresses survival, migration, and invasion of cervical cancer Chen, Xiuhui Qu, Junying Onco Targets Ther Original Research BACKGROUND: Long non-coding RNAs nowadays emerge as important biomarkers or potential therapeutic targets discussed in human cancers. Among them, maternally expressed gene 3 (MEG3) is known to be decreased in a variety of malignancies, and this affects tumor cellular proliferation, migration, and invasion. MATERIALS AND METHODS: Quantitative real-time PCR was performed to detect the expression of MEG3 in normal cervical epithelium, cervical intraepithelial neoplasia, and cervical squamous cell carcinoma tissues. Gain-of-function and loss-of-function studies were carried out to determine the effect of MEG3 on cell survival, migration, and invasion, which was evaluated by CCK-8 assay, wound healing assay, and transwell assays. mRNA and protein expression of Rac1 were finally determined by quantitative real-time PCR and immunoblotting, respectively. In addition, rescue experiments were performed by overexpression of Rac1. RESULTS: The expression of MEG3 was downregulated in cervical intraepithelial neoplasia and squamous cell carcinoma tissues. Forced expression of MEG3 led to reduced abilities of cell survival. Overexpression of MEG3 also inhibited cell migration and invasion in vitro. Cell proliferation marker and EMT markers were changed consistently with the phenotype. In addition, Rac1 was inhibited by MEG3 overexpression at both transcriptional and translational levels. Also, Rac1 could rescue the phenotype caused by long non-coding RNA MEG3. And, it negatively correlated with MEG3 expression in cervical cancer (CC) tissues and cell lines. CONCLUSION: Our findings revealed that MEG3 could negatively regulate CC cell survival, migration, and invasion. It might serve as an important target for CC treatment. Dove Medical Press 2018-08-20 /pmc/articles/PMC6109651/ /pubmed/30174437 http://dx.doi.org/10.2147/OTT.S167053 Text en © 2018 Chen and Qu. 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 Chen, Xiuhui Qu, Junying Long non-coding RNA MEG3 suppresses survival, migration, and invasion of cervical cancer |
title | Long non-coding RNA MEG3 suppresses survival, migration, and invasion of cervical cancer |
title_full | Long non-coding RNA MEG3 suppresses survival, migration, and invasion of cervical cancer |
title_fullStr | Long non-coding RNA MEG3 suppresses survival, migration, and invasion of cervical cancer |
title_full_unstemmed | Long non-coding RNA MEG3 suppresses survival, migration, and invasion of cervical cancer |
title_short | Long non-coding RNA MEG3 suppresses survival, migration, and invasion of cervical cancer |
title_sort | long non-coding rna meg3 suppresses survival, migration, and invasion of cervical cancer |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6109651/ https://www.ncbi.nlm.nih.gov/pubmed/30174437 http://dx.doi.org/10.2147/OTT.S167053 |
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