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Long Noncoding RNA CDKN2B-AS1 Facilitates Lung Cancer Development Through Regulating miR-378b/NR2C2

AIM: Long noncoding RNA (lncRNA) have proved to be important regulators in various diseases. CDKN2B-AS1 was a newly identified tumor-related lncRNA, and previous studies have reported its function in laryngeal squamous cancer and osteosarcoma. However, the function and mechanism of lncRNA CDKN2B-AS1...

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Autores principales: Wang, Guolei, Xu, Guanghui, Wang, Wenguang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7585785/
https://www.ncbi.nlm.nih.gov/pubmed/33116641
http://dx.doi.org/10.2147/OTT.S261973
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author Wang, Guolei
Xu, Guanghui
Wang, Wenguang
author_facet Wang, Guolei
Xu, Guanghui
Wang, Wenguang
author_sort Wang, Guolei
collection PubMed
description AIM: Long noncoding RNA (lncRNA) have proved to be important regulators in various diseases. CDKN2B-AS1 was a newly identified tumor-related lncRNA, and previous studies have reported its function in laryngeal squamous cancer and osteosarcoma. However, the function and mechanism of lncRNA CDKN2B-AS1 in lung cancer are still unknown. METHODS: Cell proliferation, invasion, migration and apoptosis were detected via CCK-8, transwell assay and Western blot. Bioinformatics analysis was used to predict the potential target of CDKN2B-AS1. A rescue experiment was performed to identify the relationship between CDKN2B-AS1 and miR-378b. RESULTS: The expression of lncRNA CDKN2B-AS1 was significantly upregulated in lung cancer tissues and cell lines. Overexpression of CDKN2B-AS1 promoted cell proliferation, invasion and reduced cell apoptosis. Knockdown of CDKN2B-AS1 inhibited cell proliferation, invasion and increased cell apoptosis. Bioinformatics analysis predicted that miR-378b was the direct target. We also provided evidence that NR2C2 was the target of miR-378b. The expression of NR2C2 was significantly upregulated in lung cancer tissues and cell lines. The rescue experiment further confirmed the relationship between CDKN2B-AS1 and miR-378b. Overexpression of miR-378b completely reversed the function of CDKN2B-AS1. CONCLUSION: Taken together, our results comprehensively analyzed the function of CDKN2B-AS1 in lung cancer and provided a possible mechanism that CDKN2B-AS1 facilitates lung cancer development by regulating miR-378b and NR2C2. Thus, our study offers a potential therapeutic target for treating lung cancer.
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spelling pubmed-75857852020-10-27 Long Noncoding RNA CDKN2B-AS1 Facilitates Lung Cancer Development Through Regulating miR-378b/NR2C2 Wang, Guolei Xu, Guanghui Wang, Wenguang Onco Targets Ther Original Research AIM: Long noncoding RNA (lncRNA) have proved to be important regulators in various diseases. CDKN2B-AS1 was a newly identified tumor-related lncRNA, and previous studies have reported its function in laryngeal squamous cancer and osteosarcoma. However, the function and mechanism of lncRNA CDKN2B-AS1 in lung cancer are still unknown. METHODS: Cell proliferation, invasion, migration and apoptosis were detected via CCK-8, transwell assay and Western blot. Bioinformatics analysis was used to predict the potential target of CDKN2B-AS1. A rescue experiment was performed to identify the relationship between CDKN2B-AS1 and miR-378b. RESULTS: The expression of lncRNA CDKN2B-AS1 was significantly upregulated in lung cancer tissues and cell lines. Overexpression of CDKN2B-AS1 promoted cell proliferation, invasion and reduced cell apoptosis. Knockdown of CDKN2B-AS1 inhibited cell proliferation, invasion and increased cell apoptosis. Bioinformatics analysis predicted that miR-378b was the direct target. We also provided evidence that NR2C2 was the target of miR-378b. The expression of NR2C2 was significantly upregulated in lung cancer tissues and cell lines. The rescue experiment further confirmed the relationship between CDKN2B-AS1 and miR-378b. Overexpression of miR-378b completely reversed the function of CDKN2B-AS1. CONCLUSION: Taken together, our results comprehensively analyzed the function of CDKN2B-AS1 in lung cancer and provided a possible mechanism that CDKN2B-AS1 facilitates lung cancer development by regulating miR-378b and NR2C2. Thus, our study offers a potential therapeutic target for treating lung cancer. Dove 2020-10-20 /pmc/articles/PMC7585785/ /pubmed/33116641 http://dx.doi.org/10.2147/OTT.S261973 Text en © 2020 Wang et al. http://creativecommons.org/licenses/by-nc/3.0/ 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. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Wang, Guolei
Xu, Guanghui
Wang, Wenguang
Long Noncoding RNA CDKN2B-AS1 Facilitates Lung Cancer Development Through Regulating miR-378b/NR2C2
title Long Noncoding RNA CDKN2B-AS1 Facilitates Lung Cancer Development Through Regulating miR-378b/NR2C2
title_full Long Noncoding RNA CDKN2B-AS1 Facilitates Lung Cancer Development Through Regulating miR-378b/NR2C2
title_fullStr Long Noncoding RNA CDKN2B-AS1 Facilitates Lung Cancer Development Through Regulating miR-378b/NR2C2
title_full_unstemmed Long Noncoding RNA CDKN2B-AS1 Facilitates Lung Cancer Development Through Regulating miR-378b/NR2C2
title_short Long Noncoding RNA CDKN2B-AS1 Facilitates Lung Cancer Development Through Regulating miR-378b/NR2C2
title_sort long noncoding rna cdkn2b-as1 facilitates lung cancer development through regulating mir-378b/nr2c2
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7585785/
https://www.ncbi.nlm.nih.gov/pubmed/33116641
http://dx.doi.org/10.2147/OTT.S261973
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