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Long Non-Coding RNA LINC00662 Regulated Proliferation and Migration by Targeting miR-34a-5p/LMAN2L Axis in Glioma

Authors Geng Y, Wu Y, Xu C, Li T, Zhang L

Received 21 July 2020

Accepted for publication 4 September 2020

Published 9 October 2020 Volume 2020:13 Pages 10161—10172

DOI https://doi.org/10.2147/OTT.S272616

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Prof. Dr. Nicola Silvestris


Yibo Geng,1,* Yuliang Wu,2,* Cheng Xu,1 Tian Li,1 Liwei Zhang1,3

1Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, People’s Republic of China; 2Department of Neurosurgery, Qilu Children’s Hospital, Shandong University, Jinan, Shandong, People’s Republic of China; 3China National Clinical Research Center for Neurological Disease, Beijing, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Liwei Zhang
Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, No. 119 Nan Si Huan West Road, Fengtai District, Beijing 100070, People’s Republic of China
Tel +86-15101181174
Fax +86-010-59976611
Email zhangliweittyy@163.com

Background: Numerous studies suggest that long non-coding RNAs (lncRNAs) participate in the biological process of diverse malignancies, including glioma. Although many differentially expressed lncRNAs have been identified in glioma, to our best knowledge, the role of LINC00662 and its potential underlying mechanism in glioma progression remains unclear. This study aimed to explore the function and regulatory network of LINC00662 in glioma.
Methods: Expressions of LINC00662, miR-34a-5p and lectin mannose-binding 2-like (LMAN2L) in glioma tissues were analyzed using The Cancer Genome Atlas Program (TCGA) and the Chinese Glioma Genome Atlas (CGGA) databases. Colony formation, Celltiter-Glo and BrdU (5-bromo-2ʹ-deoxyuridine) incorporation assays were used to detect cell proliferation in vitro. Xenograft mouse models were established to determine cell proliferation in vivo. Transwell and wound healing assay was used to detect cell migration. In addition, epithelial–mesenchymal transition (EMT) markers were detected by Western blot. Annexin V and 7-AAD were used to stain apoptotic cells. Interactions between miR-34a-5p and LINC00662 or the 3′-UTR of LMAN2L were predicted and determined by bioinformatics analysis, luciferase reporter assay and RNA immunoprecipitation (RIP) assays.
Results: High LINC00662 level predicted poor overall survival of glioma patients. Functional studies revealed that suppression of LINC00662 remarkably inhibited cell proliferation, clonogenicity and EMT pathway. Mechanistically, LINC00662 sponged miR-34a-5p to regulate LMAN2L expression. Furthermore, miR-34a-5p inhibitor reversed the anti-proliferation and anti-migration effect of LINC00662 knockdown, which could be rescued by downregulation of LMAN2L in glioma cells.
Conclusion: Our study was the first to report that LINC00662 acted as a competing endogenous RNA (ceRNA) to regulate glioma progression by targeting miR-34a-5p/LMAN2L axis, providing a new therapeutic target for glioma.

Keywords: long non-coding RNA, LINC00662, miR-34a-5p, LMAN2L, glioma, epithelial–mesenchymal transition

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