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LncRNA FOXD3-AS1 Promotes Tumorigenesis of Glioma via Targeting miR-128-3p/SZRD1 Axis
BACKGROUND: The aim of the current study was to investigate the roles of LncRNA FOXD3-AS1 (FOXD3-AS1) in the glioma progression, and its underlying mechanism of competing endogenous RNA (ceRNA) network of FOXD3-AS1/miR-128-3p/SZRD1. MATERIALS AND METHODS: The FOXD3-AS1 expression and its prognostic...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8666723/ https://www.ncbi.nlm.nih.gov/pubmed/34916848 http://dx.doi.org/10.2147/CMAR.S324920 |
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author | Li, Zhang Li, Ming Xia, Pengcheng Wang, Lili Lu, Zhiming |
author_facet | Li, Zhang Li, Ming Xia, Pengcheng Wang, Lili Lu, Zhiming |
author_sort | Li, Zhang |
collection | PubMed |
description | BACKGROUND: The aim of the current study was to investigate the roles of LncRNA FOXD3-AS1 (FOXD3-AS1) in the glioma progression, and its underlying mechanism of competing endogenous RNA (ceRNA) network of FOXD3-AS1/miR-128-3p/SZRD1. MATERIALS AND METHODS: The FOXD3-AS1 expression and its prognostic relation were detected by bioinformatics tool. Next, glioma cell lines (HS683, U251, T98G, and SNB-19) were used to verify the FOXD3-AS1 expression. Furthermore, the roles of the FOXD3-AS1/miR-128-3p/SZRD1 axis on the glioma development in vitro and in vivo were examined. RESULTS: Bioinformatics analysis showed that FOXD3-AS1 was upregulated in the glioma and linked with poor prognosis. Consistently, FOXD3-AS1 level was overexpressed in the glioma cell lines (HS683 and U251). Subsequently, we verified that silencing of FOXD3-AS1 (si-FOXD3-AS1) restrained the cell proliferation, invasion, and tumor growth in vivo, and induced G0/G1 arrest, and promoted apoptosis. Further study also stated that FOXD3-AS1 interacted with miR-128-3p and SZRD1 was the target gene of miR-128-3p. Moreover, overexpression of miR-128-3p restrained the cell proliferation and metastasis of glioma, and reduced the SZRD1 level. Rescue assay illustrated that miR-128-3p inhibitor could reverse the suppressive impact of si-FOXD3-AS1 on the glioma progression. Similarly, SZRD1 overexpression could neutralize the influences of miR-128-3p mimic on glioma progression. CONCLUSION: FOXD3-AS1 promoted the tumorigenesis of glioma, and exerted its function to modulate SZRD1 by targeting miR-128-3p. |
format | Online Article Text |
id | pubmed-8666723 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-86667232021-12-15 LncRNA FOXD3-AS1 Promotes Tumorigenesis of Glioma via Targeting miR-128-3p/SZRD1 Axis Li, Zhang Li, Ming Xia, Pengcheng Wang, Lili Lu, Zhiming Cancer Manag Res Original Research BACKGROUND: The aim of the current study was to investigate the roles of LncRNA FOXD3-AS1 (FOXD3-AS1) in the glioma progression, and its underlying mechanism of competing endogenous RNA (ceRNA) network of FOXD3-AS1/miR-128-3p/SZRD1. MATERIALS AND METHODS: The FOXD3-AS1 expression and its prognostic relation were detected by bioinformatics tool. Next, glioma cell lines (HS683, U251, T98G, and SNB-19) were used to verify the FOXD3-AS1 expression. Furthermore, the roles of the FOXD3-AS1/miR-128-3p/SZRD1 axis on the glioma development in vitro and in vivo were examined. RESULTS: Bioinformatics analysis showed that FOXD3-AS1 was upregulated in the glioma and linked with poor prognosis. Consistently, FOXD3-AS1 level was overexpressed in the glioma cell lines (HS683 and U251). Subsequently, we verified that silencing of FOXD3-AS1 (si-FOXD3-AS1) restrained the cell proliferation, invasion, and tumor growth in vivo, and induced G0/G1 arrest, and promoted apoptosis. Further study also stated that FOXD3-AS1 interacted with miR-128-3p and SZRD1 was the target gene of miR-128-3p. Moreover, overexpression of miR-128-3p restrained the cell proliferation and metastasis of glioma, and reduced the SZRD1 level. Rescue assay illustrated that miR-128-3p inhibitor could reverse the suppressive impact of si-FOXD3-AS1 on the glioma progression. Similarly, SZRD1 overexpression could neutralize the influences of miR-128-3p mimic on glioma progression. CONCLUSION: FOXD3-AS1 promoted the tumorigenesis of glioma, and exerted its function to modulate SZRD1 by targeting miR-128-3p. Dove 2021-12-07 /pmc/articles/PMC8666723/ /pubmed/34916848 http://dx.doi.org/10.2147/CMAR.S324920 Text en © 2021 Li et al. https://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/ (https://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 Li, Zhang Li, Ming Xia, Pengcheng Wang, Lili Lu, Zhiming LncRNA FOXD3-AS1 Promotes Tumorigenesis of Glioma via Targeting miR-128-3p/SZRD1 Axis |
title | LncRNA FOXD3-AS1 Promotes Tumorigenesis of Glioma via Targeting miR-128-3p/SZRD1 Axis |
title_full | LncRNA FOXD3-AS1 Promotes Tumorigenesis of Glioma via Targeting miR-128-3p/SZRD1 Axis |
title_fullStr | LncRNA FOXD3-AS1 Promotes Tumorigenesis of Glioma via Targeting miR-128-3p/SZRD1 Axis |
title_full_unstemmed | LncRNA FOXD3-AS1 Promotes Tumorigenesis of Glioma via Targeting miR-128-3p/SZRD1 Axis |
title_short | LncRNA FOXD3-AS1 Promotes Tumorigenesis of Glioma via Targeting miR-128-3p/SZRD1 Axis |
title_sort | lncrna foxd3-as1 promotes tumorigenesis of glioma via targeting mir-128-3p/szrd1 axis |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8666723/ https://www.ncbi.nlm.nih.gov/pubmed/34916848 http://dx.doi.org/10.2147/CMAR.S324920 |
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