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FoxD2-AS1 promotes glioma progression by regulating miR-185-5P/HMGA2 axis and PI3K/AKT signaling pathway
Background/Aims: The present study was aimed at exploring the role of long noncoding RNA (lncRNA) FOXD2-AS1 in the development and progression of glioma and the underlying mechanism of FOXD2-AS1/miR-185-5p/HMGA2 network in glioma via regulation of PI3K/Akt signaling pathway. Methods: Microarray anal...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6428107/ https://www.ncbi.nlm.nih.gov/pubmed/30860979 http://dx.doi.org/10.18632/aging.101843 |
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author | Ni, Wei Xia, Yaoxiong Bi, Yuxu Wen, Fan Hu, Dong Luo, Lin |
author_facet | Ni, Wei Xia, Yaoxiong Bi, Yuxu Wen, Fan Hu, Dong Luo, Lin |
author_sort | Ni, Wei |
collection | PubMed |
description | Background/Aims: The present study was aimed at exploring the role of long noncoding RNA (lncRNA) FOXD2-AS1 in the development and progression of glioma and the underlying mechanism of FOXD2-AS1/miR-185-5p/HMGA2 network in glioma via regulation of PI3K/Akt signaling pathway. Methods: Microarray analysis was used for preliminary screening for candidate lncRNAs and mRNAs in glioma tissues. qRT-PCR and Western blot were used to determine the expression of FOXD2-AS1. The potential effects of FOXD2-AS1 on the viability, mobility and apoptosis of glioma cells were evaluated using MTT assay, Transwell assays and flow cytometry. The xenograft tumor model was performed to examine the influence of the lncRNA FOXD2-AS1/miR-185-5p/HMGA2 network on the biological functions of glioma cells. Luciferase assay and immunoprecipitation assay were examined to dissect molecular mechanisms. Results: LncRNA FOXD2-AS1 was overexpressed in human glioma, and upregulated FOXD2-AS11 expression indicated higher WHO grade (p < 0.05). MiR-185-5p was downregulated, whereas HMGA2 was upregulated in glioma tissues in comparison with para-carcinoma tissues. FOXD2-AS1 could regulate the expression of HMGA2 via miR-185-5p. Knockdown of FOXD2-AS1 significantly inhibited proliferation and metastatic potential of glioma cells, whereas endogenous expression FOXD2-AS1 inhibited the glioma cell activity through targeting HMGA2. Conclusions: lncRNA FOXD2-AS1 acted as a sponge of miR-185-5p and influenced the PI3K/Akt signaling pathway through regulating HMGA2. LncRNA FOXD2-AS1 modulated HMGA2 and PI3K/Akt downstream signaling through sponging miR-185-5p, thereby promoting tumorigenesis and progression of glioma. |
format | Online Article Text |
id | pubmed-6428107 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Impact Journals |
record_format | MEDLINE/PubMed |
spelling | pubmed-64281072019-03-26 FoxD2-AS1 promotes glioma progression by regulating miR-185-5P/HMGA2 axis and PI3K/AKT signaling pathway Ni, Wei Xia, Yaoxiong Bi, Yuxu Wen, Fan Hu, Dong Luo, Lin Aging (Albany NY) Research Paper Background/Aims: The present study was aimed at exploring the role of long noncoding RNA (lncRNA) FOXD2-AS1 in the development and progression of glioma and the underlying mechanism of FOXD2-AS1/miR-185-5p/HMGA2 network in glioma via regulation of PI3K/Akt signaling pathway. Methods: Microarray analysis was used for preliminary screening for candidate lncRNAs and mRNAs in glioma tissues. qRT-PCR and Western blot were used to determine the expression of FOXD2-AS1. The potential effects of FOXD2-AS1 on the viability, mobility and apoptosis of glioma cells were evaluated using MTT assay, Transwell assays and flow cytometry. The xenograft tumor model was performed to examine the influence of the lncRNA FOXD2-AS1/miR-185-5p/HMGA2 network on the biological functions of glioma cells. Luciferase assay and immunoprecipitation assay were examined to dissect molecular mechanisms. Results: LncRNA FOXD2-AS1 was overexpressed in human glioma, and upregulated FOXD2-AS11 expression indicated higher WHO grade (p < 0.05). MiR-185-5p was downregulated, whereas HMGA2 was upregulated in glioma tissues in comparison with para-carcinoma tissues. FOXD2-AS1 could regulate the expression of HMGA2 via miR-185-5p. Knockdown of FOXD2-AS1 significantly inhibited proliferation and metastatic potential of glioma cells, whereas endogenous expression FOXD2-AS1 inhibited the glioma cell activity through targeting HMGA2. Conclusions: lncRNA FOXD2-AS1 acted as a sponge of miR-185-5p and influenced the PI3K/Akt signaling pathway through regulating HMGA2. LncRNA FOXD2-AS1 modulated HMGA2 and PI3K/Akt downstream signaling through sponging miR-185-5p, thereby promoting tumorigenesis and progression of glioma. Impact Journals 2019-03-11 /pmc/articles/PMC6428107/ /pubmed/30860979 http://dx.doi.org/10.18632/aging.101843 Text en Copyright © 2019 Ni et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY) 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Paper Ni, Wei Xia, Yaoxiong Bi, Yuxu Wen, Fan Hu, Dong Luo, Lin FoxD2-AS1 promotes glioma progression by regulating miR-185-5P/HMGA2 axis and PI3K/AKT signaling pathway |
title | FoxD2-AS1 promotes glioma progression by regulating miR-185-5P/HMGA2 axis and PI3K/AKT signaling pathway |
title_full | FoxD2-AS1 promotes glioma progression by regulating miR-185-5P/HMGA2 axis and PI3K/AKT signaling pathway |
title_fullStr | FoxD2-AS1 promotes glioma progression by regulating miR-185-5P/HMGA2 axis and PI3K/AKT signaling pathway |
title_full_unstemmed | FoxD2-AS1 promotes glioma progression by regulating miR-185-5P/HMGA2 axis and PI3K/AKT signaling pathway |
title_short | FoxD2-AS1 promotes glioma progression by regulating miR-185-5P/HMGA2 axis and PI3K/AKT signaling pathway |
title_sort | foxd2-as1 promotes glioma progression by regulating mir-185-5p/hmga2 axis and pi3k/akt signaling pathway |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6428107/ https://www.ncbi.nlm.nih.gov/pubmed/30860979 http://dx.doi.org/10.18632/aging.101843 |
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