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HOXA10-AS: A novel oncogenic long non-coding RNA in glioma
Glioma is the most common primary malignant tumor of the central nervous system. Emerging evidence has demonstrated that long non-coding RNAs (lncRNAs) serve a major role of regulation in various types of human cancer, including glioma. However, the biological roles of thousands of lncRNAs remain un...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6151881/ https://www.ncbi.nlm.nih.gov/pubmed/30132568 http://dx.doi.org/10.3892/or.2018.6662 |
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author | Dong, Cheng-Ya Cui, Jiayue Li, Dian-He Li, Qi Hong, Xin-Yu |
author_facet | Dong, Cheng-Ya Cui, Jiayue Li, Dian-He Li, Qi Hong, Xin-Yu |
author_sort | Dong, Cheng-Ya |
collection | PubMed |
description | Glioma is the most common primary malignant tumor of the central nervous system. Emerging evidence has demonstrated that long non-coding RNAs (lncRNAs) serve a major role of regulation in various types of human cancer, including glioma. However, the biological roles of thousands of lncRNAs remain unknown and require further identification. The present study investigated the functional role of lncRNA-HOXA10-AS in glioma. The present study examined the expression patterns of HOXA10-AS in glioma and normal brain tissues, as well as glioma cell lines and normal human astrocytes (HA) via reverse transcription-quantitative polymerase chain reaction. HOXA10-AS knockdown cells were generated using lentiviral short hairpin RNA against HOXA10-AS in A172 and U251 glioma cells. Cell growth was assessed by MTT assay, and a flow cytometer was used to investigate cell proliferation, cell cycle distribution and cell apoptosis. Western blot analysis was performed to analyze the expression levels of apoptosis-related proteins. HOXA10-AS was significantly upregulated in glioma tissues and cell lines, and increased HOXA10-AS expression levels were associated with higher grades of glioma. Knockdown of HOXA10-AS inhibited glioma cell proliferation and increased cell apoptosis rates compared with the control cells. HOXA10-AS markedly regulated the expression of the homeobox A10 (HOXA10) gene. Similarly, HOXA10 expression was increased with higher grades of glioma, and silencing of HOXA10 by small interfering RNA suppressed glioma cell proliferation and induced cell apoptosis. The results of the present study demonstrated that HOXA10-AS promoted cell growth and survival through activation of HOXA10 gene expression in glioma, which may potentially act as a novel biomarker and therapeutic target for clinical assay development. |
format | Online Article Text |
id | pubmed-6151881 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-61518812018-09-25 HOXA10-AS: A novel oncogenic long non-coding RNA in glioma Dong, Cheng-Ya Cui, Jiayue Li, Dian-He Li, Qi Hong, Xin-Yu Oncol Rep Articles Glioma is the most common primary malignant tumor of the central nervous system. Emerging evidence has demonstrated that long non-coding RNAs (lncRNAs) serve a major role of regulation in various types of human cancer, including glioma. However, the biological roles of thousands of lncRNAs remain unknown and require further identification. The present study investigated the functional role of lncRNA-HOXA10-AS in glioma. The present study examined the expression patterns of HOXA10-AS in glioma and normal brain tissues, as well as glioma cell lines and normal human astrocytes (HA) via reverse transcription-quantitative polymerase chain reaction. HOXA10-AS knockdown cells were generated using lentiviral short hairpin RNA against HOXA10-AS in A172 and U251 glioma cells. Cell growth was assessed by MTT assay, and a flow cytometer was used to investigate cell proliferation, cell cycle distribution and cell apoptosis. Western blot analysis was performed to analyze the expression levels of apoptosis-related proteins. HOXA10-AS was significantly upregulated in glioma tissues and cell lines, and increased HOXA10-AS expression levels were associated with higher grades of glioma. Knockdown of HOXA10-AS inhibited glioma cell proliferation and increased cell apoptosis rates compared with the control cells. HOXA10-AS markedly regulated the expression of the homeobox A10 (HOXA10) gene. Similarly, HOXA10 expression was increased with higher grades of glioma, and silencing of HOXA10 by small interfering RNA suppressed glioma cell proliferation and induced cell apoptosis. The results of the present study demonstrated that HOXA10-AS promoted cell growth and survival through activation of HOXA10 gene expression in glioma, which may potentially act as a novel biomarker and therapeutic target for clinical assay development. D.A. Spandidos 2018-11 2018-08-21 /pmc/articles/PMC6151881/ /pubmed/30132568 http://dx.doi.org/10.3892/or.2018.6662 Text en Copyright: © Dong et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Dong, Cheng-Ya Cui, Jiayue Li, Dian-He Li, Qi Hong, Xin-Yu HOXA10-AS: A novel oncogenic long non-coding RNA in glioma |
title | HOXA10-AS: A novel oncogenic long non-coding RNA in glioma |
title_full | HOXA10-AS: A novel oncogenic long non-coding RNA in glioma |
title_fullStr | HOXA10-AS: A novel oncogenic long non-coding RNA in glioma |
title_full_unstemmed | HOXA10-AS: A novel oncogenic long non-coding RNA in glioma |
title_short | HOXA10-AS: A novel oncogenic long non-coding RNA in glioma |
title_sort | hoxa10-as: a novel oncogenic long non-coding rna in glioma |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6151881/ https://www.ncbi.nlm.nih.gov/pubmed/30132568 http://dx.doi.org/10.3892/or.2018.6662 |
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