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Knockdown of Long Non-Coding RNA NEAT1 Inhibits Proliferation and Invasion and Induces Apoptosis of Osteosarcoma by Inhibiting miR-194 Expression
PURPOSE: Long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) has been implicated as an oncogene in the development and progression of osteosarcoma. This study aims to explore the mechanism of NEAT1 in osteosarcoma. MATERIALS AND METHODS: Expressions of NEAT1 and miR-194 in...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Yonsei University College of Medicine
2017
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5653473/ https://www.ncbi.nlm.nih.gov/pubmed/29047232 http://dx.doi.org/10.3349/ymj.2017.58.6.1092 |
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author | Wang, Heping Yu, Yanzhang Fan, Shuxin Luo, Leifeng |
author_facet | Wang, Heping Yu, Yanzhang Fan, Shuxin Luo, Leifeng |
author_sort | Wang, Heping |
collection | PubMed |
description | PURPOSE: Long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) has been implicated as an oncogene in the development and progression of osteosarcoma. This study aims to explore the mechanism of NEAT1 in osteosarcoma. MATERIALS AND METHODS: Expressions of NEAT1 and miR-194 in osteosarcoma tissues and cells were detected by quantitative real-time PCR. The effects of NEAT1 knockdown or miR-194 overexpression on cell proliferation, invasion, and apoptosis were determined by 3-[4, 5-dimethylthiazol-2-yl]-2, 5 diphenyl tetrazolium bromide (MTT) assay, transwell invasive assay, and flow cytometry analysis, respectively. Luciferase reporter assay was performed to observe the possible interaction between NEAT1 and miR-194. RESULTS: NEAT1 was upregulated and miR-194 was downregulated in osteosarcoma tissues and cells. Knockdown of NEAT1 or overexpression of miR-194 suppressed proliferation and invasion and induced apoptosis of osteosarcoma cells in vitro. Luciferase reporter assay validated that NEAT1 could interact with miR-194 and negatively modulated its expression. Furthermore, inhibition of miR-194 reversed the suppression of proliferation and invasion and the promotion of apoptosis induced by NEAT1 depletion in osteosarcoma cells. CONCLUSION: Knockdown of NEAT1 suppressed proliferation and invasion and induced apoptosis in osteosarcoma cells by inhibiting miR-194 expression. |
format | Online Article Text |
id | pubmed-5653473 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Yonsei University College of Medicine |
record_format | MEDLINE/PubMed |
spelling | pubmed-56534732017-11-01 Knockdown of Long Non-Coding RNA NEAT1 Inhibits Proliferation and Invasion and Induces Apoptosis of Osteosarcoma by Inhibiting miR-194 Expression Wang, Heping Yu, Yanzhang Fan, Shuxin Luo, Leifeng Yonsei Med J Original Article PURPOSE: Long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) has been implicated as an oncogene in the development and progression of osteosarcoma. This study aims to explore the mechanism of NEAT1 in osteosarcoma. MATERIALS AND METHODS: Expressions of NEAT1 and miR-194 in osteosarcoma tissues and cells were detected by quantitative real-time PCR. The effects of NEAT1 knockdown or miR-194 overexpression on cell proliferation, invasion, and apoptosis were determined by 3-[4, 5-dimethylthiazol-2-yl]-2, 5 diphenyl tetrazolium bromide (MTT) assay, transwell invasive assay, and flow cytometry analysis, respectively. Luciferase reporter assay was performed to observe the possible interaction between NEAT1 and miR-194. RESULTS: NEAT1 was upregulated and miR-194 was downregulated in osteosarcoma tissues and cells. Knockdown of NEAT1 or overexpression of miR-194 suppressed proliferation and invasion and induced apoptosis of osteosarcoma cells in vitro. Luciferase reporter assay validated that NEAT1 could interact with miR-194 and negatively modulated its expression. Furthermore, inhibition of miR-194 reversed the suppression of proliferation and invasion and the promotion of apoptosis induced by NEAT1 depletion in osteosarcoma cells. CONCLUSION: Knockdown of NEAT1 suppressed proliferation and invasion and induced apoptosis in osteosarcoma cells by inhibiting miR-194 expression. Yonsei University College of Medicine 2017-11-01 2017-09-28 /pmc/articles/PMC5653473/ /pubmed/29047232 http://dx.doi.org/10.3349/ymj.2017.58.6.1092 Text en © Copyright: Yonsei University College of Medicine 2017 http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Wang, Heping Yu, Yanzhang Fan, Shuxin Luo, Leifeng Knockdown of Long Non-Coding RNA NEAT1 Inhibits Proliferation and Invasion and Induces Apoptosis of Osteosarcoma by Inhibiting miR-194 Expression |
title | Knockdown of Long Non-Coding RNA NEAT1 Inhibits Proliferation and Invasion and Induces Apoptosis of Osteosarcoma by Inhibiting miR-194 Expression |
title_full | Knockdown of Long Non-Coding RNA NEAT1 Inhibits Proliferation and Invasion and Induces Apoptosis of Osteosarcoma by Inhibiting miR-194 Expression |
title_fullStr | Knockdown of Long Non-Coding RNA NEAT1 Inhibits Proliferation and Invasion and Induces Apoptosis of Osteosarcoma by Inhibiting miR-194 Expression |
title_full_unstemmed | Knockdown of Long Non-Coding RNA NEAT1 Inhibits Proliferation and Invasion and Induces Apoptosis of Osteosarcoma by Inhibiting miR-194 Expression |
title_short | Knockdown of Long Non-Coding RNA NEAT1 Inhibits Proliferation and Invasion and Induces Apoptosis of Osteosarcoma by Inhibiting miR-194 Expression |
title_sort | knockdown of long non-coding rna neat1 inhibits proliferation and invasion and induces apoptosis of osteosarcoma by inhibiting mir-194 expression |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5653473/ https://www.ncbi.nlm.nih.gov/pubmed/29047232 http://dx.doi.org/10.3349/ymj.2017.58.6.1092 |
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