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The interplay between ATF2 and NEAT1 contributes to lung adenocarcinoma progression
BACKGROUND: Activating transcription factor 2 (ATF2), a member of the activator protein 1 (AP-1) transcription factor family, has been shown to be involved in the pathobiology of numerous cancers. However, the biological role and mechanism of ATF2 in lung adenocarcinoma (LUAD) remains to be elucidat...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7727147/ https://www.ncbi.nlm.nih.gov/pubmed/33298086 http://dx.doi.org/10.1186/s12935-020-01697-8 |
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author | Liu, Jian Li, Kai Wang, Rui Chen, Sisi Wu, Jie Li, Xiang Ning, Qian Yang, Ganghua Pang, Yamei |
author_facet | Liu, Jian Li, Kai Wang, Rui Chen, Sisi Wu, Jie Li, Xiang Ning, Qian Yang, Ganghua Pang, Yamei |
author_sort | Liu, Jian |
collection | PubMed |
description | BACKGROUND: Activating transcription factor 2 (ATF2), a member of the activator protein 1 (AP-1) transcription factor family, has been shown to be involved in the pathobiology of numerous cancers. However, the biological role and mechanism of ATF2 in lung adenocarcinoma (LUAD) remains to be elucidated. METHODS: The expression of ATF2, NEAT1 and miR-26a-5p in LUAD tissues and cell lines was detected by qRT-PCR and western blotting. The interaction between ATF2, NEAT1, and miR-26a-5p was validated by chromatin immunoprecipitation, luciferase reporter assay and RNA immunoprecipitation. Cell proliferation, invasion and tumorigenesis of LUAD cells were analyzed by using CCK8, transwell invasion assay and xenograft tumor model. RESULTS: We confirmed that ATF2 expression was increased in LUAD tissues compared with normal adjacent lung tissues. Functional experiments showed that ATF2 positively regulated cell proliferation and invasion in LUAD cells. Moreover, we identified that NEAT1 expression was increased in LUAD tissues and positively correlated with ATF2 expression. Mechanistically, ATF2 could bind to the promoter of NEAT1 to promote its transcription. Rescue experiments showed that ATF2 exerted its oncogenic function in LUAD, at least, partly through NEAT1 upregulation. In turn, NEAT1 could positively regulate ATF2 expression and form a positive feedback loop in LUAD cells. Furthermore, we demonstrated that NEAT1 positively regulated ATF2 expression via sponging miR-26a-5p. CONCLUSION: ATF2 and NEAT1 form a positive feedback loop mediated by miR-26a-5p and coordinately contribute to LUAD progression. |
format | Online Article Text |
id | pubmed-7727147 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-77271472020-12-10 The interplay between ATF2 and NEAT1 contributes to lung adenocarcinoma progression Liu, Jian Li, Kai Wang, Rui Chen, Sisi Wu, Jie Li, Xiang Ning, Qian Yang, Ganghua Pang, Yamei Cancer Cell Int Primary Research BACKGROUND: Activating transcription factor 2 (ATF2), a member of the activator protein 1 (AP-1) transcription factor family, has been shown to be involved in the pathobiology of numerous cancers. However, the biological role and mechanism of ATF2 in lung adenocarcinoma (LUAD) remains to be elucidated. METHODS: The expression of ATF2, NEAT1 and miR-26a-5p in LUAD tissues and cell lines was detected by qRT-PCR and western blotting. The interaction between ATF2, NEAT1, and miR-26a-5p was validated by chromatin immunoprecipitation, luciferase reporter assay and RNA immunoprecipitation. Cell proliferation, invasion and tumorigenesis of LUAD cells were analyzed by using CCK8, transwell invasion assay and xenograft tumor model. RESULTS: We confirmed that ATF2 expression was increased in LUAD tissues compared with normal adjacent lung tissues. Functional experiments showed that ATF2 positively regulated cell proliferation and invasion in LUAD cells. Moreover, we identified that NEAT1 expression was increased in LUAD tissues and positively correlated with ATF2 expression. Mechanistically, ATF2 could bind to the promoter of NEAT1 to promote its transcription. Rescue experiments showed that ATF2 exerted its oncogenic function in LUAD, at least, partly through NEAT1 upregulation. In turn, NEAT1 could positively regulate ATF2 expression and form a positive feedback loop in LUAD cells. Furthermore, we demonstrated that NEAT1 positively regulated ATF2 expression via sponging miR-26a-5p. CONCLUSION: ATF2 and NEAT1 form a positive feedback loop mediated by miR-26a-5p and coordinately contribute to LUAD progression. BioMed Central 2020-12-09 /pmc/articles/PMC7727147/ /pubmed/33298086 http://dx.doi.org/10.1186/s12935-020-01697-8 Text en © The Author(s) 2020 Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Primary Research Liu, Jian Li, Kai Wang, Rui Chen, Sisi Wu, Jie Li, Xiang Ning, Qian Yang, Ganghua Pang, Yamei The interplay between ATF2 and NEAT1 contributes to lung adenocarcinoma progression |
title | The interplay between ATF2 and NEAT1 contributes to lung adenocarcinoma progression |
title_full | The interplay between ATF2 and NEAT1 contributes to lung adenocarcinoma progression |
title_fullStr | The interplay between ATF2 and NEAT1 contributes to lung adenocarcinoma progression |
title_full_unstemmed | The interplay between ATF2 and NEAT1 contributes to lung adenocarcinoma progression |
title_short | The interplay between ATF2 and NEAT1 contributes to lung adenocarcinoma progression |
title_sort | interplay between atf2 and neat1 contributes to lung adenocarcinoma progression |
topic | Primary Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7727147/ https://www.ncbi.nlm.nih.gov/pubmed/33298086 http://dx.doi.org/10.1186/s12935-020-01697-8 |
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