FBXL19-AS1 promotes the progression of nasopharyngeal carcinoma by acting as a competing endogenous RNA to sponge miR-431 and upregulate PBOV1

Long non-coding RNAs (lncRNAs) have been shown to function as crucial regulators in the progression of various types of cancer, including nasopharyngeal carcinoma (NPC). The aim of the present study was to investigate the mechanisms underlying the role of the FBXL19-AS1/microRNA (miR)-431/prostate a...

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Autores principales: Dong, Hongjun, Huang, Chao, Huang, Jingjing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8299196/
https://www.ncbi.nlm.nih.gov/pubmed/34278444
http://dx.doi.org/10.3892/mmr.2021.12286
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author Dong, Hongjun
Huang, Chao
Huang, Jingjing
author_facet Dong, Hongjun
Huang, Chao
Huang, Jingjing
author_sort Dong, Hongjun
collection PubMed
description Long non-coding RNAs (lncRNAs) have been shown to function as crucial regulators in the progression of various types of cancer, including nasopharyngeal carcinoma (NPC). The aim of the present study was to investigate the mechanisms underlying the role of the FBXL19-AS1/microRNA (miR)-431/prostate and breast cancer overexpressed 1 (PBOV1) axis in the progression of NPC. The expression levels of FBXL19-AS1, miR-431 and PBOV1 were assessed by reverse transcription-quantitative PCR. The Cell Counting Kit-8 assay was utilized to detect cell viability. Cell migration and invasion were determined using a Transwell assay. The associations between FBXL19-AS1 and miR-431 or miR-431 and PBOV1 were verified via bioinformatics analysis, dual-luciferase and RNA-binding protein immunoprecipitation assays. It was demonstrated that the expression levels of FBXL19-AS1 and PBOV1 were upregulated in NPC tissues and cells, whereas miR-431 expression was downregulated. FBXL19-AS1 directly interacted with miR-431. FBXL19-AS1 silencing inhibited the viability, migration and invasion of C666-1 and SUNE1 cells, whereas these effects could be alleviated by suppressing miR-431. miR-431 could target the 3′-untranslated region of PBOV1. Overexpression of PBOV1 neutralized the miR-431-mediated suppression of NPC progression. Moreover, FBXL19-AS1 could regulate PBOV1 by sponging miR-431 in NPC cells. In conclusion, the lncRNA FBXL19-AS1 accelerated NPC progression via the miR-431/PBOV1 axis, suggesting that it may serve as a potential therapeutic target for patients with NPC.
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spelling pubmed-82991962021-08-11 FBXL19-AS1 promotes the progression of nasopharyngeal carcinoma by acting as a competing endogenous RNA to sponge miR-431 and upregulate PBOV1 Dong, Hongjun Huang, Chao Huang, Jingjing Mol Med Rep Articles Long non-coding RNAs (lncRNAs) have been shown to function as crucial regulators in the progression of various types of cancer, including nasopharyngeal carcinoma (NPC). The aim of the present study was to investigate the mechanisms underlying the role of the FBXL19-AS1/microRNA (miR)-431/prostate and breast cancer overexpressed 1 (PBOV1) axis in the progression of NPC. The expression levels of FBXL19-AS1, miR-431 and PBOV1 were assessed by reverse transcription-quantitative PCR. The Cell Counting Kit-8 assay was utilized to detect cell viability. Cell migration and invasion were determined using a Transwell assay. The associations between FBXL19-AS1 and miR-431 or miR-431 and PBOV1 were verified via bioinformatics analysis, dual-luciferase and RNA-binding protein immunoprecipitation assays. It was demonstrated that the expression levels of FBXL19-AS1 and PBOV1 were upregulated in NPC tissues and cells, whereas miR-431 expression was downregulated. FBXL19-AS1 directly interacted with miR-431. FBXL19-AS1 silencing inhibited the viability, migration and invasion of C666-1 and SUNE1 cells, whereas these effects could be alleviated by suppressing miR-431. miR-431 could target the 3′-untranslated region of PBOV1. Overexpression of PBOV1 neutralized the miR-431-mediated suppression of NPC progression. Moreover, FBXL19-AS1 could regulate PBOV1 by sponging miR-431 in NPC cells. In conclusion, the lncRNA FBXL19-AS1 accelerated NPC progression via the miR-431/PBOV1 axis, suggesting that it may serve as a potential therapeutic target for patients with NPC. D.A. Spandidos 2021-09 2021-07-12 /pmc/articles/PMC8299196/ /pubmed/34278444 http://dx.doi.org/10.3892/mmr.2021.12286 Text en Copyright: © Dong et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , 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 Articles
Dong, Hongjun
Huang, Chao
Huang, Jingjing
FBXL19-AS1 promotes the progression of nasopharyngeal carcinoma by acting as a competing endogenous RNA to sponge miR-431 and upregulate PBOV1
title FBXL19-AS1 promotes the progression of nasopharyngeal carcinoma by acting as a competing endogenous RNA to sponge miR-431 and upregulate PBOV1
title_full FBXL19-AS1 promotes the progression of nasopharyngeal carcinoma by acting as a competing endogenous RNA to sponge miR-431 and upregulate PBOV1
title_fullStr FBXL19-AS1 promotes the progression of nasopharyngeal carcinoma by acting as a competing endogenous RNA to sponge miR-431 and upregulate PBOV1
title_full_unstemmed FBXL19-AS1 promotes the progression of nasopharyngeal carcinoma by acting as a competing endogenous RNA to sponge miR-431 and upregulate PBOV1
title_short FBXL19-AS1 promotes the progression of nasopharyngeal carcinoma by acting as a competing endogenous RNA to sponge miR-431 and upregulate PBOV1
title_sort fbxl19-as1 promotes the progression of nasopharyngeal carcinoma by acting as a competing endogenous rna to sponge mir-431 and upregulate pbov1
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8299196/
https://www.ncbi.nlm.nih.gov/pubmed/34278444
http://dx.doi.org/10.3892/mmr.2021.12286
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