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Long non-coding RNA LINC01419 mediates miR-519a-3p/PDRG1 axis to promote cell progression in osteosarcoma

BACKGROUND: Osteosarcoma (OS) is one of the most aggressive malignancies with mortality rate worldwide. Accumulating evidence has revealed that long noncoding RNAs (lncRNAs) exert important functions in regulation of cancer initiation and progression. Recently, long intergenic non-protein coding RNA...

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Autores principales: Gu, Zhiqian, Wu, Shaokun, Wang, Jingnan, Zhao, Shoujun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7201774/
https://www.ncbi.nlm.nih.gov/pubmed/32390762
http://dx.doi.org/10.1186/s12935-020-01203-0
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author Gu, Zhiqian
Wu, Shaokun
Wang, Jingnan
Zhao, Shoujun
author_facet Gu, Zhiqian
Wu, Shaokun
Wang, Jingnan
Zhao, Shoujun
author_sort Gu, Zhiqian
collection PubMed
description BACKGROUND: Osteosarcoma (OS) is one of the most aggressive malignancies with mortality rate worldwide. Accumulating evidence has revealed that long noncoding RNAs (lncRNAs) exert important functions in regulation of cancer initiation and progression. Recently, long intergenic non-protein coding RNA 1419 (LINC01419) has been reported to function as an oncogene in several cancers. However, its role in OS has not been explored yet. METHODS: qRT-PCR and western blot analyses were implemented to determine the expression of genes. The function of OS cells was assessed through colony formation, EdU, JC-1, TUNEL, transwell, and immunofluorescence (IF) assays. FISH and subcellular fractionation assays were conducted to estimate the localization of LINC01419 in OS cells. The interaction between genes was validated through luciferase reporter and RNA pull down assays. RESULTS: LINC01419 expression was elevated in OS tissues and cells. Functionally, LINC01419 accelerated OS cell proliferation, motility and EMT. In vivo assay showed that silencing LINC01419 hindered the growth of OS tumors. Mechanistic investigation unveiled that LINC01419 acted as a competing endogenous RNA (ceRNA) to augment PDRG1 expression by miR-519a-3p sequestration. Rescue assays verified the oncogenic effect of LINC01419/miR-519a-3p/PDRG1 axis on OS development. CONCLUSION: LINC01419 mediates malignant phenotypes in OS by targeting miR-519a-3p/PDRG1 axis.
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spelling pubmed-72017742020-05-08 Long non-coding RNA LINC01419 mediates miR-519a-3p/PDRG1 axis to promote cell progression in osteosarcoma Gu, Zhiqian Wu, Shaokun Wang, Jingnan Zhao, Shoujun Cancer Cell Int Primary Research BACKGROUND: Osteosarcoma (OS) is one of the most aggressive malignancies with mortality rate worldwide. Accumulating evidence has revealed that long noncoding RNAs (lncRNAs) exert important functions in regulation of cancer initiation and progression. Recently, long intergenic non-protein coding RNA 1419 (LINC01419) has been reported to function as an oncogene in several cancers. However, its role in OS has not been explored yet. METHODS: qRT-PCR and western blot analyses were implemented to determine the expression of genes. The function of OS cells was assessed through colony formation, EdU, JC-1, TUNEL, transwell, and immunofluorescence (IF) assays. FISH and subcellular fractionation assays were conducted to estimate the localization of LINC01419 in OS cells. The interaction between genes was validated through luciferase reporter and RNA pull down assays. RESULTS: LINC01419 expression was elevated in OS tissues and cells. Functionally, LINC01419 accelerated OS cell proliferation, motility and EMT. In vivo assay showed that silencing LINC01419 hindered the growth of OS tumors. Mechanistic investigation unveiled that LINC01419 acted as a competing endogenous RNA (ceRNA) to augment PDRG1 expression by miR-519a-3p sequestration. Rescue assays verified the oncogenic effect of LINC01419/miR-519a-3p/PDRG1 axis on OS development. CONCLUSION: LINC01419 mediates malignant phenotypes in OS by targeting miR-519a-3p/PDRG1 axis. BioMed Central 2020-05-05 /pmc/articles/PMC7201774/ /pubmed/32390762 http://dx.doi.org/10.1186/s12935-020-01203-0 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
Gu, Zhiqian
Wu, Shaokun
Wang, Jingnan
Zhao, Shoujun
Long non-coding RNA LINC01419 mediates miR-519a-3p/PDRG1 axis to promote cell progression in osteosarcoma
title Long non-coding RNA LINC01419 mediates miR-519a-3p/PDRG1 axis to promote cell progression in osteosarcoma
title_full Long non-coding RNA LINC01419 mediates miR-519a-3p/PDRG1 axis to promote cell progression in osteosarcoma
title_fullStr Long non-coding RNA LINC01419 mediates miR-519a-3p/PDRG1 axis to promote cell progression in osteosarcoma
title_full_unstemmed Long non-coding RNA LINC01419 mediates miR-519a-3p/PDRG1 axis to promote cell progression in osteosarcoma
title_short Long non-coding RNA LINC01419 mediates miR-519a-3p/PDRG1 axis to promote cell progression in osteosarcoma
title_sort long non-coding rna linc01419 mediates mir-519a-3p/pdrg1 axis to promote cell progression in osteosarcoma
topic Primary Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7201774/
https://www.ncbi.nlm.nih.gov/pubmed/32390762
http://dx.doi.org/10.1186/s12935-020-01203-0
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