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Long Noncoding RNA NEAT1 Suppresses Proliferation and Promotes Apoptosis of Glioma Cells Via Downregulating MiR-92b
BACKGROUND: The mechanisms underlying the proliferation and apoptosis of glioma cells remain unelucidated. A recent study has revealed that microRNA-92b (miR-92b) inhibits apoptosis of glioma cells via downregulating DKK3. Notably, long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) is...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6961147/ https://www.ncbi.nlm.nih.gov/pubmed/31933377 http://dx.doi.org/10.1177/1073274819897977 |
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author | Liu, Dongdong Zou, Zheng Li, Gen Pan, Pengyu Liang, Guobiao |
author_facet | Liu, Dongdong Zou, Zheng Li, Gen Pan, Pengyu Liang, Guobiao |
author_sort | Liu, Dongdong |
collection | PubMed |
description | BACKGROUND: The mechanisms underlying the proliferation and apoptosis of glioma cells remain unelucidated. A recent study has revealed that microRNA-92b (miR-92b) inhibits apoptosis of glioma cells via downregulating DKK3. Notably, long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) is predicted to have a possible interaction with miR-92b. OBJECTIVE: This study aimed to identify whether NEAT1 affects glioma cell proliferation and apoptosis via regulating miR-92b. METHODS: The expression of NEAT1 was compared between glioma tissues and adjacent tissues as well as between glioma cells and normal astrocytes using quantitative real-time polymerase chain reaction. Glioma cell proliferation was determined by using the 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and glioma cell apoptosis was determined by using the flow cytometry. RESULTS: The expression of NEAT1 was low in glioma tissues and cells compared to the normal ones. Overexpression of NEAT1 inhibited proliferation and promoted apoptosis of glioma cell lines (U-87 MG and U251). The interaction between NEAT1 and miR-92b was confirmed using RNA immunoprecipitation, RNA pull-down assay, and luciferase reporter assay. Importantly, the tumor suppressor function of overexpressing NEAT1 was achieved by downregulating miR-92b and subsequently upregulating DKK3. CONCLUSION: Our findings indicated that NEAT1 acts as a tumor suppressor in glioma cells, which provides a novel target in overcoming glioma growth. |
format | Online Article Text |
id | pubmed-6961147 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-69611472020-01-24 Long Noncoding RNA NEAT1 Suppresses Proliferation and Promotes Apoptosis of Glioma Cells Via Downregulating MiR-92b Liu, Dongdong Zou, Zheng Li, Gen Pan, Pengyu Liang, Guobiao Cancer Control Research Article BACKGROUND: The mechanisms underlying the proliferation and apoptosis of glioma cells remain unelucidated. A recent study has revealed that microRNA-92b (miR-92b) inhibits apoptosis of glioma cells via downregulating DKK3. Notably, long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) is predicted to have a possible interaction with miR-92b. OBJECTIVE: This study aimed to identify whether NEAT1 affects glioma cell proliferation and apoptosis via regulating miR-92b. METHODS: The expression of NEAT1 was compared between glioma tissues and adjacent tissues as well as between glioma cells and normal astrocytes using quantitative real-time polymerase chain reaction. Glioma cell proliferation was determined by using the 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and glioma cell apoptosis was determined by using the flow cytometry. RESULTS: The expression of NEAT1 was low in glioma tissues and cells compared to the normal ones. Overexpression of NEAT1 inhibited proliferation and promoted apoptosis of glioma cell lines (U-87 MG and U251). The interaction between NEAT1 and miR-92b was confirmed using RNA immunoprecipitation, RNA pull-down assay, and luciferase reporter assay. Importantly, the tumor suppressor function of overexpressing NEAT1 was achieved by downregulating miR-92b and subsequently upregulating DKK3. CONCLUSION: Our findings indicated that NEAT1 acts as a tumor suppressor in glioma cells, which provides a novel target in overcoming glioma growth. SAGE Publications 2020-01-14 /pmc/articles/PMC6961147/ /pubmed/31933377 http://dx.doi.org/10.1177/1073274819897977 Text en © The Author(s) 2020 https://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Research Article Liu, Dongdong Zou, Zheng Li, Gen Pan, Pengyu Liang, Guobiao Long Noncoding RNA NEAT1 Suppresses Proliferation and Promotes Apoptosis of Glioma Cells Via Downregulating MiR-92b |
title | Long Noncoding RNA NEAT1 Suppresses Proliferation and Promotes
Apoptosis of Glioma Cells Via Downregulating MiR-92b |
title_full | Long Noncoding RNA NEAT1 Suppresses Proliferation and Promotes
Apoptosis of Glioma Cells Via Downregulating MiR-92b |
title_fullStr | Long Noncoding RNA NEAT1 Suppresses Proliferation and Promotes
Apoptosis of Glioma Cells Via Downregulating MiR-92b |
title_full_unstemmed | Long Noncoding RNA NEAT1 Suppresses Proliferation and Promotes
Apoptosis of Glioma Cells Via Downregulating MiR-92b |
title_short | Long Noncoding RNA NEAT1 Suppresses Proliferation and Promotes
Apoptosis of Glioma Cells Via Downregulating MiR-92b |
title_sort | long noncoding rna neat1 suppresses proliferation and promotes
apoptosis of glioma cells via downregulating mir-92b |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6961147/ https://www.ncbi.nlm.nih.gov/pubmed/31933377 http://dx.doi.org/10.1177/1073274819897977 |
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