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Long Noncoding RNA FGD5-AS1 Promotes Glioma Cell Proliferation, Migration and Invasion by Regulating wnt/β-Catenin Pathway

PURPOSE: To investigate the specific function of long noncoding RNA FGD5 antisense RNA 1 (lncRNA FGD5-AS1) in glioma. MATERIALS AND METHODS: The level of FGD5-AS1 was detected in clinical samples and cell lines by qRT-PCR. Small interfering RNA (siRNA) of FGD5-AS1 or scramble siRNA was transfected i...

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Autores principales: Zhao, Jun Bo, Xue, Jun Feng, Zhang, Wu Zhong, Ren, Yong Lu, Yan, Dong Ming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7398887/
https://www.ncbi.nlm.nih.gov/pubmed/32801867
http://dx.doi.org/10.2147/CMAR.S250284
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author Zhao, Jun Bo
Xue, Jun Feng
Zhang, Wu Zhong
Ren, Yong Lu
Yan, Dong Ming
author_facet Zhao, Jun Bo
Xue, Jun Feng
Zhang, Wu Zhong
Ren, Yong Lu
Yan, Dong Ming
author_sort Zhao, Jun Bo
collection PubMed
description PURPOSE: To investigate the specific function of long noncoding RNA FGD5 antisense RNA 1 (lncRNA FGD5-AS1) in glioma. MATERIALS AND METHODS: The level of FGD5-AS1 was detected in clinical samples and cell lines by qRT-PCR. Small interfering RNA (siRNA) of FGD5-AS1 or scramble siRNA was transfected into U87 cell lines to examine the role of FGD5-AS1 on glioma development. The proliferation of glioma cells was tested by Cell Counting Kit-8 (CCK-8), the migration and invasion of glioma cells were tested by transwell assay without matrigel or with matrigel. Western blot was used to detect the protein expression, and XAV-939 was used to inhibit wnt/β-catenin pathway. The effect of FGD5-AS1 on tumorigenesis of glioma was confirmed by xenograft nude mice model. RESULTS: FGD5-AS1 was significantly increased in glioma tissues and cells. Loss of FGD5-AS1 inhibited the proliferation, migration and invasion of U87 cells. Furthermore, overexpression of FGD5-AS1 increased the mRNA and protein levels of β-catenin and cyclin D1. Blocking of wnt/β-catenin using XAV-939 reversed the promotion role of FGD3-AS1 on glioma cells’ migration and invasion. The in vivo tumor growth assay showed that FGD3-AS1 accelerated glioma tumorigenesis with activating wnt/β-catenin pathway. CONCLUSION: Our research emphasized FGD5-AS1 acting as an oncogene by regulating wnt/β-catenin signaling pathway, thus providing some novel experimental basis for clinical treatment of glioma.
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spelling pubmed-73988872020-08-14 Long Noncoding RNA FGD5-AS1 Promotes Glioma Cell Proliferation, Migration and Invasion by Regulating wnt/β-Catenin Pathway Zhao, Jun Bo Xue, Jun Feng Zhang, Wu Zhong Ren, Yong Lu Yan, Dong Ming Cancer Manag Res Original Research PURPOSE: To investigate the specific function of long noncoding RNA FGD5 antisense RNA 1 (lncRNA FGD5-AS1) in glioma. MATERIALS AND METHODS: The level of FGD5-AS1 was detected in clinical samples and cell lines by qRT-PCR. Small interfering RNA (siRNA) of FGD5-AS1 or scramble siRNA was transfected into U87 cell lines to examine the role of FGD5-AS1 on glioma development. The proliferation of glioma cells was tested by Cell Counting Kit-8 (CCK-8), the migration and invasion of glioma cells were tested by transwell assay without matrigel or with matrigel. Western blot was used to detect the protein expression, and XAV-939 was used to inhibit wnt/β-catenin pathway. The effect of FGD5-AS1 on tumorigenesis of glioma was confirmed by xenograft nude mice model. RESULTS: FGD5-AS1 was significantly increased in glioma tissues and cells. Loss of FGD5-AS1 inhibited the proliferation, migration and invasion of U87 cells. Furthermore, overexpression of FGD5-AS1 increased the mRNA and protein levels of β-catenin and cyclin D1. Blocking of wnt/β-catenin using XAV-939 reversed the promotion role of FGD3-AS1 on glioma cells’ migration and invasion. The in vivo tumor growth assay showed that FGD3-AS1 accelerated glioma tumorigenesis with activating wnt/β-catenin pathway. CONCLUSION: Our research emphasized FGD5-AS1 acting as an oncogene by regulating wnt/β-catenin signaling pathway, thus providing some novel experimental basis for clinical treatment of glioma. Dove 2020-07-23 /pmc/articles/PMC7398887/ /pubmed/32801867 http://dx.doi.org/10.2147/CMAR.S250284 Text en © 2020 Zhao 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
Zhao, Jun Bo
Xue, Jun Feng
Zhang, Wu Zhong
Ren, Yong Lu
Yan, Dong Ming
Long Noncoding RNA FGD5-AS1 Promotes Glioma Cell Proliferation, Migration and Invasion by Regulating wnt/β-Catenin Pathway
title Long Noncoding RNA FGD5-AS1 Promotes Glioma Cell Proliferation, Migration and Invasion by Regulating wnt/β-Catenin Pathway
title_full Long Noncoding RNA FGD5-AS1 Promotes Glioma Cell Proliferation, Migration and Invasion by Regulating wnt/β-Catenin Pathway
title_fullStr Long Noncoding RNA FGD5-AS1 Promotes Glioma Cell Proliferation, Migration and Invasion by Regulating wnt/β-Catenin Pathway
title_full_unstemmed Long Noncoding RNA FGD5-AS1 Promotes Glioma Cell Proliferation, Migration and Invasion by Regulating wnt/β-Catenin Pathway
title_short Long Noncoding RNA FGD5-AS1 Promotes Glioma Cell Proliferation, Migration and Invasion by Regulating wnt/β-Catenin Pathway
title_sort long noncoding rna fgd5-as1 promotes glioma cell proliferation, migration and invasion by regulating wnt/β-catenin pathway
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7398887/
https://www.ncbi.nlm.nih.gov/pubmed/32801867
http://dx.doi.org/10.2147/CMAR.S250284
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