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Long Noncoding RNA SNHG6 Functions as an Oncogene in Non-Small Cell Lung Cancer via Modulating ETS1 Signaling
BACKGROUND: Non-small cell lung cancer (NSCLC) is a great threat to human health and the biology of the NSCLC still remains largely unknown. Aberrantly expressed long non-coding RNA (lncRNA) Small nucleolar RNA host gene 6 (SNHG6) was involved in the tumorigenesis and progression of various cancers....
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996613/ https://www.ncbi.nlm.nih.gov/pubmed/32099396 http://dx.doi.org/10.2147/OTT.S235336 |
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author | Geng, Hua Li, Shixiong Xu, Meilin |
author_facet | Geng, Hua Li, Shixiong Xu, Meilin |
author_sort | Geng, Hua |
collection | PubMed |
description | BACKGROUND: Non-small cell lung cancer (NSCLC) is a great threat to human health and the biology of the NSCLC still remains largely unknown. Aberrantly expressed long non-coding RNA (lncRNA) Small nucleolar RNA host gene 6 (SNHG6) was involved in the tumorigenesis and progression of various cancers. The aim of this study is to investigate the roles of SNHG6 in NSCLC. METHODS: qRT-PCR and Western blot assays were applied to detect gene expressions. Cell proliferation and migration assays were used to analyze the gene functions. Luciferase reporter assay, RNA Immunoprecipitation assay and Chromatin immunoprecipitation assay were performed to investigate the molecular mechanism. RESULTS: We found that SNHG6 expression was significantly increased in NSCLC tissues and cell lines and its high expression was correlated with malignant features of NSCLC. In in vitro assays, knockdown of SNHG6 significantly depressed the proliferation vitality and migration activity of NSCLC cells. Research on mechanisms revealed that SNHG6 exerted its tumorigenesis role by promoting ETS1 expression via competitively binding with miR-944 and miR-181d-5p. We also demonstrated that ETS1 enhanced the expression of WIPF1 via binding to its promoter and SNHG6 could thereby regulate the expression of ETS1 target genes including WIPF1, MMP2 and MMP9. CONCLUSION: Our study illustrates that SNHG6 is an oncogene in NSCLC and involved in NSCLC tumorigenesis by regulating ETS1 signaling via miR-944 and miR-181d-5p. |
format | Online Article Text |
id | pubmed-6996613 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-69966132020-02-25 Long Noncoding RNA SNHG6 Functions as an Oncogene in Non-Small Cell Lung Cancer via Modulating ETS1 Signaling Geng, Hua Li, Shixiong Xu, Meilin Onco Targets Ther Original Research BACKGROUND: Non-small cell lung cancer (NSCLC) is a great threat to human health and the biology of the NSCLC still remains largely unknown. Aberrantly expressed long non-coding RNA (lncRNA) Small nucleolar RNA host gene 6 (SNHG6) was involved in the tumorigenesis and progression of various cancers. The aim of this study is to investigate the roles of SNHG6 in NSCLC. METHODS: qRT-PCR and Western blot assays were applied to detect gene expressions. Cell proliferation and migration assays were used to analyze the gene functions. Luciferase reporter assay, RNA Immunoprecipitation assay and Chromatin immunoprecipitation assay were performed to investigate the molecular mechanism. RESULTS: We found that SNHG6 expression was significantly increased in NSCLC tissues and cell lines and its high expression was correlated with malignant features of NSCLC. In in vitro assays, knockdown of SNHG6 significantly depressed the proliferation vitality and migration activity of NSCLC cells. Research on mechanisms revealed that SNHG6 exerted its tumorigenesis role by promoting ETS1 expression via competitively binding with miR-944 and miR-181d-5p. We also demonstrated that ETS1 enhanced the expression of WIPF1 via binding to its promoter and SNHG6 could thereby regulate the expression of ETS1 target genes including WIPF1, MMP2 and MMP9. CONCLUSION: Our study illustrates that SNHG6 is an oncogene in NSCLC and involved in NSCLC tumorigenesis by regulating ETS1 signaling via miR-944 and miR-181d-5p. Dove 2020-01-30 /pmc/articles/PMC6996613/ /pubmed/32099396 http://dx.doi.org/10.2147/OTT.S235336 Text en © 2020 Geng 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 Geng, Hua Li, Shixiong Xu, Meilin Long Noncoding RNA SNHG6 Functions as an Oncogene in Non-Small Cell Lung Cancer via Modulating ETS1 Signaling |
title | Long Noncoding RNA SNHG6 Functions as an Oncogene in Non-Small Cell Lung Cancer via Modulating ETS1 Signaling |
title_full | Long Noncoding RNA SNHG6 Functions as an Oncogene in Non-Small Cell Lung Cancer via Modulating ETS1 Signaling |
title_fullStr | Long Noncoding RNA SNHG6 Functions as an Oncogene in Non-Small Cell Lung Cancer via Modulating ETS1 Signaling |
title_full_unstemmed | Long Noncoding RNA SNHG6 Functions as an Oncogene in Non-Small Cell Lung Cancer via Modulating ETS1 Signaling |
title_short | Long Noncoding RNA SNHG6 Functions as an Oncogene in Non-Small Cell Lung Cancer via Modulating ETS1 Signaling |
title_sort | long noncoding rna snhg6 functions as an oncogene in non-small cell lung cancer via modulating ets1 signaling |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996613/ https://www.ncbi.nlm.nih.gov/pubmed/32099396 http://dx.doi.org/10.2147/OTT.S235336 |
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