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Long noncoding RNA OIP5-AS1 targets Wnt-7b to affect glioma progression via modulation of miR-410
The present study was undertaken to investigate the underlying mechanisms of long noncoding RNA OIP5-AS1 via regulating miR-410 to modulate Wnt-7b in the progression of glioma. To address this problem, we measured the expression of OIP5-AS1 and miR-410 in glioma tissues by qRT-PCR. Glioma U87 cells...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Portland Press Ltd.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6328889/ https://www.ncbi.nlm.nih.gov/pubmed/30498093 http://dx.doi.org/10.1042/BSR20180395 |
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author | Sun, Wei-Li Kang, Tian Wang, Yuan-Yu Sun, Jian-Ping Li, Chen Liu, Hong-Jiang Yang, Yue Jiao, Bao-Hua |
author_facet | Sun, Wei-Li Kang, Tian Wang, Yuan-Yu Sun, Jian-Ping Li, Chen Liu, Hong-Jiang Yang, Yue Jiao, Bao-Hua |
author_sort | Sun, Wei-Li |
collection | PubMed |
description | The present study was undertaken to investigate the underlying mechanisms of long noncoding RNA OIP5-AS1 via regulating miR-410 to modulate Wnt-7b in the progression of glioma. To address this problem, we measured the expression of OIP5-AS1 and miR-410 in glioma tissues by qRT-PCR. Glioma U87 cells were transfected with OIP5-AS1 siRNA or miR-410 inhibitors. The targeting relationships among miR-410, OIP5-AS1 and Wnt-7b were verified by luciferase reporter assays. Western blotting was employed to determine the expression of Wnt-7b/β-catenin pathway-related proteins, while MTT, flow cytometry, Transwell assays and wound-healing assays were used to measure the biological characteristics of glioma cells. The results showed that OIP5-AS1 expression was higher and miR-410 was lower in glioma tissues. Luciferase reporter assays confirmed a targeting relationship between OIP5-AS1 and miR-410, as well as between miR-410 and Wnt-7b. Silencing OIP5-AS1 reduced cell proliferation, invasion and migration of glioma U87 cells and led to depressed expression levels of miR-410, Wnt-7b, p-β-catenin, GSK-3β-pS9, c-Myc and cyclin D1. Furthermore, down-regulation of OIP5-AS1 induced G0/G1 phase cell cycle arrest and apoptosis of glioma cells. Inhibitors of miR-410 abolished the biological effects of OIP5-AS1 siRNA in glioma cells. In vivo, OIP5-AS1 knockdown also inhibited tumor growth. Taken together, this research suggested that silencing OIP5-AS1 may specifically block the Wnt-7b/β-catenin pathway via targeted up-regulating miR-410, thereby inhibiting growth, invasion and migration while promoting apoptosis in glioma cells. |
format | Online Article Text |
id | pubmed-6328889 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Portland Press Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-63288892019-01-18 Long noncoding RNA OIP5-AS1 targets Wnt-7b to affect glioma progression via modulation of miR-410 Sun, Wei-Li Kang, Tian Wang, Yuan-Yu Sun, Jian-Ping Li, Chen Liu, Hong-Jiang Yang, Yue Jiao, Bao-Hua Biosci Rep Research Articles The present study was undertaken to investigate the underlying mechanisms of long noncoding RNA OIP5-AS1 via regulating miR-410 to modulate Wnt-7b in the progression of glioma. To address this problem, we measured the expression of OIP5-AS1 and miR-410 in glioma tissues by qRT-PCR. Glioma U87 cells were transfected with OIP5-AS1 siRNA or miR-410 inhibitors. The targeting relationships among miR-410, OIP5-AS1 and Wnt-7b were verified by luciferase reporter assays. Western blotting was employed to determine the expression of Wnt-7b/β-catenin pathway-related proteins, while MTT, flow cytometry, Transwell assays and wound-healing assays were used to measure the biological characteristics of glioma cells. The results showed that OIP5-AS1 expression was higher and miR-410 was lower in glioma tissues. Luciferase reporter assays confirmed a targeting relationship between OIP5-AS1 and miR-410, as well as between miR-410 and Wnt-7b. Silencing OIP5-AS1 reduced cell proliferation, invasion and migration of glioma U87 cells and led to depressed expression levels of miR-410, Wnt-7b, p-β-catenin, GSK-3β-pS9, c-Myc and cyclin D1. Furthermore, down-regulation of OIP5-AS1 induced G0/G1 phase cell cycle arrest and apoptosis of glioma cells. Inhibitors of miR-410 abolished the biological effects of OIP5-AS1 siRNA in glioma cells. In vivo, OIP5-AS1 knockdown also inhibited tumor growth. Taken together, this research suggested that silencing OIP5-AS1 may specifically block the Wnt-7b/β-catenin pathway via targeted up-regulating miR-410, thereby inhibiting growth, invasion and migration while promoting apoptosis in glioma cells. Portland Press Ltd. 2019-01-03 /pmc/articles/PMC6328889/ /pubmed/30498093 http://dx.doi.org/10.1042/BSR20180395 Text en © 2019 The Author(s). http://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (http://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Research Articles Sun, Wei-Li Kang, Tian Wang, Yuan-Yu Sun, Jian-Ping Li, Chen Liu, Hong-Jiang Yang, Yue Jiao, Bao-Hua Long noncoding RNA OIP5-AS1 targets Wnt-7b to affect glioma progression via modulation of miR-410 |
title | Long noncoding RNA OIP5-AS1 targets Wnt-7b to affect glioma progression via modulation of miR-410 |
title_full | Long noncoding RNA OIP5-AS1 targets Wnt-7b to affect glioma progression via modulation of miR-410 |
title_fullStr | Long noncoding RNA OIP5-AS1 targets Wnt-7b to affect glioma progression via modulation of miR-410 |
title_full_unstemmed | Long noncoding RNA OIP5-AS1 targets Wnt-7b to affect glioma progression via modulation of miR-410 |
title_short | Long noncoding RNA OIP5-AS1 targets Wnt-7b to affect glioma progression via modulation of miR-410 |
title_sort | long noncoding rna oip5-as1 targets wnt-7b to affect glioma progression via modulation of mir-410 |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6328889/ https://www.ncbi.nlm.nih.gov/pubmed/30498093 http://dx.doi.org/10.1042/BSR20180395 |
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