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Long non-coding RNA MEG3 suppresses survival, migration, and invasion of cervical cancer

Authors Chen X, Qu J

Received 1 March 2018

Accepted for publication 23 May 2018

Published 20 August 2018 Volume 2018:11 Pages 4999—5007

DOI https://doi.org/10.2147/OTT.S167053

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Colin Mak

Peer reviewer comments 2

Editor who approved publication: Prof. Dr. Geoffrey Pietersz


Xiuhui Chen,1 Junying Qu2

1Department of Obstetrics and Gynecology, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200021, China; 2Department of Obstetrics and Gynecology, 1st Affiliated Hospital of Fujian Medical University, Fuzhou 350005, China

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.

Keywords: MEG3, cervical cancer, survival, migration and invasion, Rac1

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