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LINC01503/miR-342-3p facilitates malignancy in non-small-cell lung cancer cells via regulating LASP1
BACKGROUND: Non-small cell lung cancer (NSCLC) is one of the major types of lung cancer, which is a prevalent human disease all over the world. LncRNA LINC01503 is a super-enhancer-driven long non-coding RNA that is dysregulated in several types of human cancer. However, its role in NSCLC remains un...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7493870/ https://www.ncbi.nlm.nih.gov/pubmed/32938459 http://dx.doi.org/10.1186/s12931-020-01464-3 |
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author | Shen, Qiming Sun, Yanbin Xu, Shun |
author_facet | Shen, Qiming Sun, Yanbin Xu, Shun |
author_sort | Shen, Qiming |
collection | PubMed |
description | BACKGROUND: Non-small cell lung cancer (NSCLC) is one of the major types of lung cancer, which is a prevalent human disease all over the world. LncRNA LINC01503 is a super-enhancer-driven long non-coding RNA that is dysregulated in several types of human cancer. However, its role in NSCLC remains unknown. METHODS: Thirty NSCLC patients were recruited between April 2012 and April 2016. Luciferase reporter assay, qRT-PCR, Cell Counting Kit-8 (CCK-8), Transwell migration assay, RNA pull-down assay, western blotting, 5-ethynyl-29-deoxyuridine (EdU) assays, and flow cytometry were utilized to characterize the roles and relationships among LINC01503, miR-342-3p, and LASP1 in NSCLC. The transplanted mouse model was built to examine their biological functions in vivo. RESULTS: We demonstrated that the expression of lncRNA LINC01503 and LIM and SH3 domain protein 1 (LASP1) were upregulated and miR-342-3p was downregulated in NSCLC samples and cell lines. Functional experiments revealed that inhibiting the expression of LINC01503 or over-expression of miR-342-3p inhibited NSCLC growth and metastasis both in vitro and in vivo. In addition, LINC01503 could bind to miR-342-3p and affect the expression of LASP1. CONCLUSION: These results provide a comprehensive analysis of the roles of LINC01503 as a competing endogenous RNA (ceRNA) in NSCLC progression. |
format | Online Article Text |
id | pubmed-7493870 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-74938702020-09-23 LINC01503/miR-342-3p facilitates malignancy in non-small-cell lung cancer cells via regulating LASP1 Shen, Qiming Sun, Yanbin Xu, Shun Respir Res Research BACKGROUND: Non-small cell lung cancer (NSCLC) is one of the major types of lung cancer, which is a prevalent human disease all over the world. LncRNA LINC01503 is a super-enhancer-driven long non-coding RNA that is dysregulated in several types of human cancer. However, its role in NSCLC remains unknown. METHODS: Thirty NSCLC patients were recruited between April 2012 and April 2016. Luciferase reporter assay, qRT-PCR, Cell Counting Kit-8 (CCK-8), Transwell migration assay, RNA pull-down assay, western blotting, 5-ethynyl-29-deoxyuridine (EdU) assays, and flow cytometry were utilized to characterize the roles and relationships among LINC01503, miR-342-3p, and LASP1 in NSCLC. The transplanted mouse model was built to examine their biological functions in vivo. RESULTS: We demonstrated that the expression of lncRNA LINC01503 and LIM and SH3 domain protein 1 (LASP1) were upregulated and miR-342-3p was downregulated in NSCLC samples and cell lines. Functional experiments revealed that inhibiting the expression of LINC01503 or over-expression of miR-342-3p inhibited NSCLC growth and metastasis both in vitro and in vivo. In addition, LINC01503 could bind to miR-342-3p and affect the expression of LASP1. CONCLUSION: These results provide a comprehensive analysis of the roles of LINC01503 as a competing endogenous RNA (ceRNA) in NSCLC progression. BioMed Central 2020-09-16 2020 /pmc/articles/PMC7493870/ /pubmed/32938459 http://dx.doi.org/10.1186/s12931-020-01464-3 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 | Research Shen, Qiming Sun, Yanbin Xu, Shun LINC01503/miR-342-3p facilitates malignancy in non-small-cell lung cancer cells via regulating LASP1 |
title | LINC01503/miR-342-3p facilitates malignancy in non-small-cell lung cancer cells via regulating LASP1 |
title_full | LINC01503/miR-342-3p facilitates malignancy in non-small-cell lung cancer cells via regulating LASP1 |
title_fullStr | LINC01503/miR-342-3p facilitates malignancy in non-small-cell lung cancer cells via regulating LASP1 |
title_full_unstemmed | LINC01503/miR-342-3p facilitates malignancy in non-small-cell lung cancer cells via regulating LASP1 |
title_short | LINC01503/miR-342-3p facilitates malignancy in non-small-cell lung cancer cells via regulating LASP1 |
title_sort | linc01503/mir-342-3p facilitates malignancy in non-small-cell lung cancer cells via regulating lasp1 |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7493870/ https://www.ncbi.nlm.nih.gov/pubmed/32938459 http://dx.doi.org/10.1186/s12931-020-01464-3 |
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