Gene amplification-driven lncRNA SNHG6 promotes tumorigenesis via epigenetically suppressing p27 expression and regulating cell cycle in non–small cell lung cancer

Long non-coding RNAs (lncRNAs) have been validated to play essential roles in non-small cell lung carcinoma (NSCLC) progression. In this study, through systematically screening GSE33532 and GSE29249 from Gene Expression Omnibus (GEO) database and bioinformatics analysis, we found the significant upr...

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Autores principales: Wang, Qi, Zhang, Wei, Yin, Dandan, Tang, Zaibin, Zhang, Erbao, Wu, Weibing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2022
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9734177/
https://www.ncbi.nlm.nih.gov/pubmed/36494339
http://dx.doi.org/10.1038/s41420-022-01276-y
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author Wang, Qi
Zhang, Wei
Yin, Dandan
Tang, Zaibin
Zhang, Erbao
Wu, Weibing
author_facet Wang, Qi
Zhang, Wei
Yin, Dandan
Tang, Zaibin
Zhang, Erbao
Wu, Weibing
author_sort Wang, Qi
collection PubMed
description Long non-coding RNAs (lncRNAs) have been validated to play essential roles in non-small cell lung carcinoma (NSCLC) progression. In this study, through systematically screening GSE33532 and GSE29249 from Gene Expression Omnibus (GEO) database and bioinformatics analysis, we found the significant upregulation of SNHG6 in NSCLC. The activation of SNHG6 was driven by copy number amplification and high expression of SNHG6 indicated a poor prognosis. Functionally, the knockdown of SNHG6 inhibited NSCLC cell proliferation, migration, and suppressed the G1/S transition of the cell cycle. SNHG6 overexpression had the opposite effects. Mechanically, SNHG6 recruited EZH2 to the promoter region of p27 and increased H3K27me3 enrichment, thus epigenetically repressing the expression of p27, regulating the cell cycle, and promoting tumorigenesis of NSCLC. SNHG6 silencing restrained tumor growth in vivo and suppressed the expressions of cell cycle-related proteins in the G1/S transition. In conclusion, our study uncovered a novel mechanism of SNHG6 activation and its function. SNHG6 can be considered a potential target for the diagnosis and treatment of NSCLC in the future.
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spelling pubmed-97341772022-12-11 Gene amplification-driven lncRNA SNHG6 promotes tumorigenesis via epigenetically suppressing p27 expression and regulating cell cycle in non–small cell lung cancer Wang, Qi Zhang, Wei Yin, Dandan Tang, Zaibin Zhang, Erbao Wu, Weibing Cell Death Discov Article Long non-coding RNAs (lncRNAs) have been validated to play essential roles in non-small cell lung carcinoma (NSCLC) progression. In this study, through systematically screening GSE33532 and GSE29249 from Gene Expression Omnibus (GEO) database and bioinformatics analysis, we found the significant upregulation of SNHG6 in NSCLC. The activation of SNHG6 was driven by copy number amplification and high expression of SNHG6 indicated a poor prognosis. Functionally, the knockdown of SNHG6 inhibited NSCLC cell proliferation, migration, and suppressed the G1/S transition of the cell cycle. SNHG6 overexpression had the opposite effects. Mechanically, SNHG6 recruited EZH2 to the promoter region of p27 and increased H3K27me3 enrichment, thus epigenetically repressing the expression of p27, regulating the cell cycle, and promoting tumorigenesis of NSCLC. SNHG6 silencing restrained tumor growth in vivo and suppressed the expressions of cell cycle-related proteins in the G1/S transition. In conclusion, our study uncovered a novel mechanism of SNHG6 activation and its function. SNHG6 can be considered a potential target for the diagnosis and treatment of NSCLC in the future. Nature Publishing Group UK 2022-12-09 /pmc/articles/PMC9734177/ /pubmed/36494339 http://dx.doi.org/10.1038/s41420-022-01276-y Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Wang, Qi
Zhang, Wei
Yin, Dandan
Tang, Zaibin
Zhang, Erbao
Wu, Weibing
Gene amplification-driven lncRNA SNHG6 promotes tumorigenesis via epigenetically suppressing p27 expression and regulating cell cycle in non–small cell lung cancer
title Gene amplification-driven lncRNA SNHG6 promotes tumorigenesis via epigenetically suppressing p27 expression and regulating cell cycle in non–small cell lung cancer
title_full Gene amplification-driven lncRNA SNHG6 promotes tumorigenesis via epigenetically suppressing p27 expression and regulating cell cycle in non–small cell lung cancer
title_fullStr Gene amplification-driven lncRNA SNHG6 promotes tumorigenesis via epigenetically suppressing p27 expression and regulating cell cycle in non–small cell lung cancer
title_full_unstemmed Gene amplification-driven lncRNA SNHG6 promotes tumorigenesis via epigenetically suppressing p27 expression and regulating cell cycle in non–small cell lung cancer
title_short Gene amplification-driven lncRNA SNHG6 promotes tumorigenesis via epigenetically suppressing p27 expression and regulating cell cycle in non–small cell lung cancer
title_sort gene amplification-driven lncrna snhg6 promotes tumorigenesis via epigenetically suppressing p27 expression and regulating cell cycle in non–small cell lung cancer
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9734177/
https://www.ncbi.nlm.nih.gov/pubmed/36494339
http://dx.doi.org/10.1038/s41420-022-01276-y
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