Cargando…

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

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 unde...

Descripción completa

Detalles Bibliográficos
Autores principales: Geng, Yibo, Wu, Yuliang, Xu, Cheng, Li, Tian, Zhang, Liwei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7553658/
https://www.ncbi.nlm.nih.gov/pubmed/33116598
http://dx.doi.org/10.2147/OTT.S272616
_version_ 1783593649998659584
author Geng, Yibo
Wu, Yuliang
Xu, Cheng
Li, Tian
Zhang, Liwei
author_facet Geng, Yibo
Wu, Yuliang
Xu, Cheng
Li, Tian
Zhang, Liwei
author_sort Geng, Yibo
collection PubMed
description 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.
format Online
Article
Text
id pubmed-7553658
institution National Center for Biotechnology Information
language English
publishDate 2020
publisher Dove
record_format MEDLINE/PubMed
spelling pubmed-75536582020-10-27 Long Non-Coding RNA LINC00662 Regulated Proliferation and Migration by Targeting miR-34a-5p/LMAN2L Axis in Glioma Geng, Yibo Wu, Yuliang Xu, Cheng Li, Tian Zhang, Liwei Onco Targets Ther Original Research 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. Dove 2020-10-09 /pmc/articles/PMC7553658/ /pubmed/33116598 http://dx.doi.org/10.2147/OTT.S272616 Text en © 2020 Geng 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
Geng, Yibo
Wu, Yuliang
Xu, Cheng
Li, Tian
Zhang, Liwei
Long Non-Coding RNA LINC00662 Regulated Proliferation and Migration by Targeting miR-34a-5p/LMAN2L Axis in Glioma
title Long Non-Coding RNA LINC00662 Regulated Proliferation and Migration by Targeting miR-34a-5p/LMAN2L Axis in Glioma
title_full Long Non-Coding RNA LINC00662 Regulated Proliferation and Migration by Targeting miR-34a-5p/LMAN2L Axis in Glioma
title_fullStr Long Non-Coding RNA LINC00662 Regulated Proliferation and Migration by Targeting miR-34a-5p/LMAN2L Axis in Glioma
title_full_unstemmed Long Non-Coding RNA LINC00662 Regulated Proliferation and Migration by Targeting miR-34a-5p/LMAN2L Axis in Glioma
title_short Long Non-Coding RNA LINC00662 Regulated Proliferation and Migration by Targeting miR-34a-5p/LMAN2L Axis in Glioma
title_sort long non-coding rna linc00662 regulated proliferation and migration by targeting mir-34a-5p/lman2l axis in glioma
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7553658/
https://www.ncbi.nlm.nih.gov/pubmed/33116598
http://dx.doi.org/10.2147/OTT.S272616
work_keys_str_mv AT gengyibo longnoncodingrnalinc00662regulatedproliferationandmigrationbytargetingmir34a5plman2laxisinglioma
AT wuyuliang longnoncodingrnalinc00662regulatedproliferationandmigrationbytargetingmir34a5plman2laxisinglioma
AT xucheng longnoncodingrnalinc00662regulatedproliferationandmigrationbytargetingmir34a5plman2laxisinglioma
AT litian longnoncodingrnalinc00662regulatedproliferationandmigrationbytargetingmir34a5plman2laxisinglioma
AT zhangliwei longnoncodingrnalinc00662regulatedproliferationandmigrationbytargetingmir34a5plman2laxisinglioma