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LncRNA DLGAP1‐AS1 accelerates glioblastoma cell proliferation through targeting miR‐515‐5p/ROCK1/NFE2L1 axis and activating Wnt signaling pathway
INTRODUCTION: Glioblastoma (GBM), the primary malignant tumor in the central nervous system, features high aggressiveness and mortality. Long noncoding RNAs (lncRNAs) can exert the crucial function in regulating various human diseases, including GBM. However, the function and mechanism of lncRNA DLG...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8553332/ https://www.ncbi.nlm.nih.gov/pubmed/34536977 http://dx.doi.org/10.1002/brb3.2321 |
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author | Wang, Zixuan Han, Yipeng Li, Qifeng Wang, Baocheng Ma, Jie |
author_facet | Wang, Zixuan Han, Yipeng Li, Qifeng Wang, Baocheng Ma, Jie |
author_sort | Wang, Zixuan |
collection | PubMed |
description | INTRODUCTION: Glioblastoma (GBM), the primary malignant tumor in the central nervous system, features high aggressiveness and mortality. Long noncoding RNAs (lncRNAs) can exert the crucial function in regulating various human diseases, including GBM. However, the function and mechanism of lncRNA DLGAP1 antisense RNA 1 (DLGAP1‐AS1) in GBM remain still unknown. METHODS: DLGAP1‐AS1 expression in GBM cells was detected by RT‐qPCR. Functional assays were conducted to determine GBM cell proliferation and apoptosis. RIP, RNA pull down, and luciferase reporter assay were applied for measuring the interplay of DLGAP1‐AS1 with other RNAs. RESULTS: DLGAP1‐AS1 was distinctly upregulated in GBM cells. DLGAP1‐AS1 depletion inhibited cell proliferation, but induced apoptosis. MiR‐515‐5p could be sponged by DLGAP1‐AS1 in GBM cells and to repress cell proliferation in GBM. Further, Rho‐associated coiled‐coil containing protein kinase 1 (ROCK1) and Nuclear factor erythroid‐2 like 1 (NFE2L1) were confirmed as the target gene of miR‐515‐5p. Wnt signaling pathway could be activated by DLGAP1‐AS1 via regulating ROCK1 and NFE2L1 expression. Rescue assays proved that overexpression of both ROCK1 and NFE2L1 could totally reverse the inhibitory effect of silencing DLGAP1‐AS1 on GBM cell proliferation. CONCLUSION: LncRNA DLGAP1‐AS1 accelerated cell proliferation in GBM via targeting miR‐515‐5p/ROCK1/NFE2L1 axis and activating Wnt signaling pathway. |
format | Online Article Text |
id | pubmed-8553332 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-85533322021-11-04 LncRNA DLGAP1‐AS1 accelerates glioblastoma cell proliferation through targeting miR‐515‐5p/ROCK1/NFE2L1 axis and activating Wnt signaling pathway Wang, Zixuan Han, Yipeng Li, Qifeng Wang, Baocheng Ma, Jie Brain Behav Original Research INTRODUCTION: Glioblastoma (GBM), the primary malignant tumor in the central nervous system, features high aggressiveness and mortality. Long noncoding RNAs (lncRNAs) can exert the crucial function in regulating various human diseases, including GBM. However, the function and mechanism of lncRNA DLGAP1 antisense RNA 1 (DLGAP1‐AS1) in GBM remain still unknown. METHODS: DLGAP1‐AS1 expression in GBM cells was detected by RT‐qPCR. Functional assays were conducted to determine GBM cell proliferation and apoptosis. RIP, RNA pull down, and luciferase reporter assay were applied for measuring the interplay of DLGAP1‐AS1 with other RNAs. RESULTS: DLGAP1‐AS1 was distinctly upregulated in GBM cells. DLGAP1‐AS1 depletion inhibited cell proliferation, but induced apoptosis. MiR‐515‐5p could be sponged by DLGAP1‐AS1 in GBM cells and to repress cell proliferation in GBM. Further, Rho‐associated coiled‐coil containing protein kinase 1 (ROCK1) and Nuclear factor erythroid‐2 like 1 (NFE2L1) were confirmed as the target gene of miR‐515‐5p. Wnt signaling pathway could be activated by DLGAP1‐AS1 via regulating ROCK1 and NFE2L1 expression. Rescue assays proved that overexpression of both ROCK1 and NFE2L1 could totally reverse the inhibitory effect of silencing DLGAP1‐AS1 on GBM cell proliferation. CONCLUSION: LncRNA DLGAP1‐AS1 accelerated cell proliferation in GBM via targeting miR‐515‐5p/ROCK1/NFE2L1 axis and activating Wnt signaling pathway. John Wiley and Sons Inc. 2021-09-18 /pmc/articles/PMC8553332/ /pubmed/34536977 http://dx.doi.org/10.1002/brb3.2321 Text en © 2021 The Authors. Brain and Behavior published by Wiley Periodicals LLC https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Research Wang, Zixuan Han, Yipeng Li, Qifeng Wang, Baocheng Ma, Jie LncRNA DLGAP1‐AS1 accelerates glioblastoma cell proliferation through targeting miR‐515‐5p/ROCK1/NFE2L1 axis and activating Wnt signaling pathway |
title | LncRNA DLGAP1‐AS1 accelerates glioblastoma cell proliferation through targeting miR‐515‐5p/ROCK1/NFE2L1 axis and activating Wnt signaling pathway |
title_full | LncRNA DLGAP1‐AS1 accelerates glioblastoma cell proliferation through targeting miR‐515‐5p/ROCK1/NFE2L1 axis and activating Wnt signaling pathway |
title_fullStr | LncRNA DLGAP1‐AS1 accelerates glioblastoma cell proliferation through targeting miR‐515‐5p/ROCK1/NFE2L1 axis and activating Wnt signaling pathway |
title_full_unstemmed | LncRNA DLGAP1‐AS1 accelerates glioblastoma cell proliferation through targeting miR‐515‐5p/ROCK1/NFE2L1 axis and activating Wnt signaling pathway |
title_short | LncRNA DLGAP1‐AS1 accelerates glioblastoma cell proliferation through targeting miR‐515‐5p/ROCK1/NFE2L1 axis and activating Wnt signaling pathway |
title_sort | lncrna dlgap1‐as1 accelerates glioblastoma cell proliferation through targeting mir‐515‐5p/rock1/nfe2l1 axis and activating wnt signaling pathway |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8553332/ https://www.ncbi.nlm.nih.gov/pubmed/34536977 http://dx.doi.org/10.1002/brb3.2321 |
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