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NEAT1 regulates cell proliferation and apoptosis of ovarian cancer by miR-34a-5p/BCL2
BACKGROUND: Nuclear enriched abundant transcript 1 (NEAT1) has been demonstrated to act as a tumor inhibitor in many cancers. However, the role of NEAT1 in the development of ovarian cancer (OC) remains far from being elaborated. Hence, the aim of this study is to investigate the expression and func...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Dove Medical Press
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5640398/ https://www.ncbi.nlm.nih.gov/pubmed/29062236 http://dx.doi.org/10.2147/OTT.S142446 |
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author | Ding, Nan Wu, Haiying Tao, Tao Peng, Erxuan |
author_facet | Ding, Nan Wu, Haiying Tao, Tao Peng, Erxuan |
author_sort | Ding, Nan |
collection | PubMed |
description | BACKGROUND: Nuclear enriched abundant transcript 1 (NEAT1) has been demonstrated to act as a tumor inhibitor in many cancers. However, the role of NEAT1 in the development of ovarian cancer (OC) remains far from being elaborated. Hence, the aim of this study is to investigate the expression and function of NEAT1 in OC. MATERIALS AND METHODS: The expression level of NEAT1 was determined by quantitative real-time polymerase chain reaction in OC cell lines. MTT assay, caspase-3 activity assay, and flow cytometry analysis were conducted to investigate the effects of NEAT1, miR-34a-5p, or B-cell lymphoma-2 (BCL2) on OC cell proliferation and apoptosis. Luciferase reporter assay was used to confirm the interaction of NEAT1, BCL2, and miR-34a-5p in OC cells. RESULTS: NEAT1 was significantly upregulated in OC cell lines. NEAT1 overexpression promoted proliferation by increasing the proportion of cells in S phase and suppressed apoptosis of OC cells, while knockdown of NEAT1 had the opposite effect. In addition, NEAT1 was demonstrated to directly interact with miR-34a-5p and exert its oncogenic role in OC by negatively regulating miR-34a-5p. Moreover, miR-34a-5p could directly target BCL2 and suppressed its expression. miR-34a-5p overexpression suppressed OC cell proliferation and triggered apoptosis by targeting BCL2. Furthermore, NEAT1 knockdown suppressed BCL2 expression, while anti-miR-34a-5p dramatically abated the inhibitory effect of si-NEAT1 on BCL2 expression. CONCLUSION: NEAT1 regulated proliferation and apoptosis of OC cells by miR-34a-5p/BCL2, providing a potential therapeutic approach for the treatment of OC patients. |
format | Online Article Text |
id | pubmed-5640398 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-56403982017-10-23 NEAT1 regulates cell proliferation and apoptosis of ovarian cancer by miR-34a-5p/BCL2 Ding, Nan Wu, Haiying Tao, Tao Peng, Erxuan Onco Targets Ther Original Research BACKGROUND: Nuclear enriched abundant transcript 1 (NEAT1) has been demonstrated to act as a tumor inhibitor in many cancers. However, the role of NEAT1 in the development of ovarian cancer (OC) remains far from being elaborated. Hence, the aim of this study is to investigate the expression and function of NEAT1 in OC. MATERIALS AND METHODS: The expression level of NEAT1 was determined by quantitative real-time polymerase chain reaction in OC cell lines. MTT assay, caspase-3 activity assay, and flow cytometry analysis were conducted to investigate the effects of NEAT1, miR-34a-5p, or B-cell lymphoma-2 (BCL2) on OC cell proliferation and apoptosis. Luciferase reporter assay was used to confirm the interaction of NEAT1, BCL2, and miR-34a-5p in OC cells. RESULTS: NEAT1 was significantly upregulated in OC cell lines. NEAT1 overexpression promoted proliferation by increasing the proportion of cells in S phase and suppressed apoptosis of OC cells, while knockdown of NEAT1 had the opposite effect. In addition, NEAT1 was demonstrated to directly interact with miR-34a-5p and exert its oncogenic role in OC by negatively regulating miR-34a-5p. Moreover, miR-34a-5p could directly target BCL2 and suppressed its expression. miR-34a-5p overexpression suppressed OC cell proliferation and triggered apoptosis by targeting BCL2. Furthermore, NEAT1 knockdown suppressed BCL2 expression, while anti-miR-34a-5p dramatically abated the inhibitory effect of si-NEAT1 on BCL2 expression. CONCLUSION: NEAT1 regulated proliferation and apoptosis of OC cells by miR-34a-5p/BCL2, providing a potential therapeutic approach for the treatment of OC patients. Dove Medical Press 2017-10-06 /pmc/articles/PMC5640398/ /pubmed/29062236 http://dx.doi.org/10.2147/OTT.S142446 Text en © 2017 Ding et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. |
spellingShingle | Original Research Ding, Nan Wu, Haiying Tao, Tao Peng, Erxuan NEAT1 regulates cell proliferation and apoptosis of ovarian cancer by miR-34a-5p/BCL2 |
title | NEAT1 regulates cell proliferation and apoptosis of ovarian cancer by miR-34a-5p/BCL2 |
title_full | NEAT1 regulates cell proliferation and apoptosis of ovarian cancer by miR-34a-5p/BCL2 |
title_fullStr | NEAT1 regulates cell proliferation and apoptosis of ovarian cancer by miR-34a-5p/BCL2 |
title_full_unstemmed | NEAT1 regulates cell proliferation and apoptosis of ovarian cancer by miR-34a-5p/BCL2 |
title_short | NEAT1 regulates cell proliferation and apoptosis of ovarian cancer by miR-34a-5p/BCL2 |
title_sort | neat1 regulates cell proliferation and apoptosis of ovarian cancer by mir-34a-5p/bcl2 |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5640398/ https://www.ncbi.nlm.nih.gov/pubmed/29062236 http://dx.doi.org/10.2147/OTT.S142446 |
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