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LncRNA FOXP4‐AS promotes the progression of non‐small cell lung cancer by regulating the miR‐3184‐5p/EIF5A axis
Long non coding RNA FOXP4‐AS1 exerted crucial functions in various human cancers, while its role in non‐small cell lung cancer (NSCLC) remains unclear. A total of 30 pairs of NSCLC tissues and matched adjacent normal tissues were used to evaluate the expression of FOXP4‐AS1 and miR‐3184‐5p. Cell pro...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9306595/ https://www.ncbi.nlm.nih.gov/pubmed/34921595 http://dx.doi.org/10.1002/term.3275 |
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author | Li, Dingbiao Li, Zhenhua YanFei, Wang Wang, Ying Shi, Jianlin Liu, Chang Qu, Laihao Deng, Shoujun Xiong, Dalin |
author_facet | Li, Dingbiao Li, Zhenhua YanFei, Wang Wang, Ying Shi, Jianlin Liu, Chang Qu, Laihao Deng, Shoujun Xiong, Dalin |
author_sort | Li, Dingbiao |
collection | PubMed |
description | Long non coding RNA FOXP4‐AS1 exerted crucial functions in various human cancers, while its role in non‐small cell lung cancer (NSCLC) remains unclear. A total of 30 pairs of NSCLC tissues and matched adjacent normal tissues were used to evaluate the expression of FOXP4‐AS1 and miR‐3184‐5p. Cell proliferation was assessed by CCK‐8 assay and colony formation assay. Cell apoptosis was measured by flow cytometry. Bioinformatic analysis and luciferase reporter assay were performed to determine the regulatory relationship among FOXP4‐AS1, miR‐3184‐5p and EIF5A. The xenograft tumor model was constructed to confirm the function of FOXP4‐AS1 in NSCLC progression. The results showed that FOXP4‐AS1 was upregulated and miR‐3184‐5p was downregulated in NSCLC tissues and cell lines. Downregulation of FOXP4‐AS1 significantly reduced cell proliferation and induced apoptosis of NSCLC cells in vitro. FOXP4‐AS1 could regulated the expression of EIF5A by binding to miR‐3184‐5p. Rescue experiments showed that downregulation of miR‐3184‐5p or overexpression of EIF5A obviously attenuated the inhibitory effects of si‐FOXP4‐AS1 on cell proliferation, as well as the stimulating effects on cell apoptosis. Moreover, knockdown of FOXP4‐AS1 could efficiently inhibited tumor development of NSCLC in vivo. Downregulation of FOXP4‐AS1 attenuated the progression of NSCLC by regulating miR‐3184‐5p and EIF5A. |
format | Online Article Text |
id | pubmed-9306595 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-93065952022-07-28 LncRNA FOXP4‐AS promotes the progression of non‐small cell lung cancer by regulating the miR‐3184‐5p/EIF5A axis Li, Dingbiao Li, Zhenhua YanFei, Wang Wang, Ying Shi, Jianlin Liu, Chang Qu, Laihao Deng, Shoujun Xiong, Dalin J Tissue Eng Regen Med Research Articles Long non coding RNA FOXP4‐AS1 exerted crucial functions in various human cancers, while its role in non‐small cell lung cancer (NSCLC) remains unclear. A total of 30 pairs of NSCLC tissues and matched adjacent normal tissues were used to evaluate the expression of FOXP4‐AS1 and miR‐3184‐5p. Cell proliferation was assessed by CCK‐8 assay and colony formation assay. Cell apoptosis was measured by flow cytometry. Bioinformatic analysis and luciferase reporter assay were performed to determine the regulatory relationship among FOXP4‐AS1, miR‐3184‐5p and EIF5A. The xenograft tumor model was constructed to confirm the function of FOXP4‐AS1 in NSCLC progression. The results showed that FOXP4‐AS1 was upregulated and miR‐3184‐5p was downregulated in NSCLC tissues and cell lines. Downregulation of FOXP4‐AS1 significantly reduced cell proliferation and induced apoptosis of NSCLC cells in vitro. FOXP4‐AS1 could regulated the expression of EIF5A by binding to miR‐3184‐5p. Rescue experiments showed that downregulation of miR‐3184‐5p or overexpression of EIF5A obviously attenuated the inhibitory effects of si‐FOXP4‐AS1 on cell proliferation, as well as the stimulating effects on cell apoptosis. Moreover, knockdown of FOXP4‐AS1 could efficiently inhibited tumor development of NSCLC in vivo. Downregulation of FOXP4‐AS1 attenuated the progression of NSCLC by regulating miR‐3184‐5p and EIF5A. John Wiley and Sons Inc. 2022-01-22 2022-04 /pmc/articles/PMC9306595/ /pubmed/34921595 http://dx.doi.org/10.1002/term.3275 Text en © 2021 The Authors. Journal of Tissue Engineering and Regenerative Medicine published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | Research Articles Li, Dingbiao Li, Zhenhua YanFei, Wang Wang, Ying Shi, Jianlin Liu, Chang Qu, Laihao Deng, Shoujun Xiong, Dalin LncRNA FOXP4‐AS promotes the progression of non‐small cell lung cancer by regulating the miR‐3184‐5p/EIF5A axis |
title | LncRNA FOXP4‐AS promotes the progression of non‐small cell lung cancer by regulating the miR‐3184‐5p/EIF5A axis |
title_full | LncRNA FOXP4‐AS promotes the progression of non‐small cell lung cancer by regulating the miR‐3184‐5p/EIF5A axis |
title_fullStr | LncRNA FOXP4‐AS promotes the progression of non‐small cell lung cancer by regulating the miR‐3184‐5p/EIF5A axis |
title_full_unstemmed | LncRNA FOXP4‐AS promotes the progression of non‐small cell lung cancer by regulating the miR‐3184‐5p/EIF5A axis |
title_short | LncRNA FOXP4‐AS promotes the progression of non‐small cell lung cancer by regulating the miR‐3184‐5p/EIF5A axis |
title_sort | lncrna foxp4‐as promotes the progression of non‐small cell lung cancer by regulating the mir‐3184‐5p/eif5a axis |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9306595/ https://www.ncbi.nlm.nih.gov/pubmed/34921595 http://dx.doi.org/10.1002/term.3275 |
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