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LncRNA MIR17HG inhibits non-small cell lung cancer by upregulating miR-142-3p to downregulate Bach-1

BACKGROUND: This study aimed to investigate the role of MIR17HG in non-small cell lung cancer (NSCLC). METHODS: Differential expression of MIR17HG in NSCLC was first detected by exploring the TCGA dataset. Expression levels of miR-142-3p in both NSCLC and non-tumor tissues were determined by qPCR. T...

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Autores principales: Wei, Sen, Liu, Jinghao, Li, Xin, Liu, Xingyu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7104535/
https://www.ncbi.nlm.nih.gov/pubmed/32228546
http://dx.doi.org/10.1186/s12890-020-1112-3
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author Wei, Sen
Liu, Jinghao
Li, Xin
Liu, Xingyu
author_facet Wei, Sen
Liu, Jinghao
Li, Xin
Liu, Xingyu
author_sort Wei, Sen
collection PubMed
description BACKGROUND: This study aimed to investigate the role of MIR17HG in non-small cell lung cancer (NSCLC). METHODS: Differential expression of MIR17HG in NSCLC was first detected by exploring the TCGA dataset. Expression levels of miR-142-3p in both NSCLC and non-tumor tissues were determined by qPCR. The effects of overexpressing MIR17HG on the methylation of miR-142 were assessed by MSP. The effects of overexpressing MIR17HG, miR-142-3p and Bach-1 on the invasion and migration of NSCLC cells were assessed by Trasnwell invasion or migration assay. RESULTS: Analysis of TCGA dataset revealed slightly downregulated expression of MIR17HG in NSCLC. This downregulation was further confirmed by measuring the expression levels of MIR17HG in NSCLC and non-tumor tissues from NSCLC patients. MIR17HG was found to decrease the methylation of miR-142-3p, and overexpression of MIR17HG led to upregulated miR-142-3p. Moreover, overexpression of MIR17HG also led to downregulated Bach-1, the downstream target of miR-142-3p. Cell invasion and migration analysis showed that overexpression of MIR17HG and miR-142-3p led to inhibited cancer cell invasion and migration. In contrast, overexpression of Bach-1 played an opposite role and attenuated the effects of overexpressing MIR17HG and miR-142-3p. CONCLUSION: MIR17HG inhibits NSCLC by upregulating miR-142-3p to downregulate Bach-1. TRIAL REGISTRATION: TJ-MU-2012-0148594, registered January 2, 2012
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spelling pubmed-71045352020-03-31 LncRNA MIR17HG inhibits non-small cell lung cancer by upregulating miR-142-3p to downregulate Bach-1 Wei, Sen Liu, Jinghao Li, Xin Liu, Xingyu BMC Pulm Med Research Article BACKGROUND: This study aimed to investigate the role of MIR17HG in non-small cell lung cancer (NSCLC). METHODS: Differential expression of MIR17HG in NSCLC was first detected by exploring the TCGA dataset. Expression levels of miR-142-3p in both NSCLC and non-tumor tissues were determined by qPCR. The effects of overexpressing MIR17HG on the methylation of miR-142 were assessed by MSP. The effects of overexpressing MIR17HG, miR-142-3p and Bach-1 on the invasion and migration of NSCLC cells were assessed by Trasnwell invasion or migration assay. RESULTS: Analysis of TCGA dataset revealed slightly downregulated expression of MIR17HG in NSCLC. This downregulation was further confirmed by measuring the expression levels of MIR17HG in NSCLC and non-tumor tissues from NSCLC patients. MIR17HG was found to decrease the methylation of miR-142-3p, and overexpression of MIR17HG led to upregulated miR-142-3p. Moreover, overexpression of MIR17HG also led to downregulated Bach-1, the downstream target of miR-142-3p. Cell invasion and migration analysis showed that overexpression of MIR17HG and miR-142-3p led to inhibited cancer cell invasion and migration. In contrast, overexpression of Bach-1 played an opposite role and attenuated the effects of overexpressing MIR17HG and miR-142-3p. CONCLUSION: MIR17HG inhibits NSCLC by upregulating miR-142-3p to downregulate Bach-1. TRIAL REGISTRATION: TJ-MU-2012-0148594, registered January 2, 2012 BioMed Central 2020-03-30 /pmc/articles/PMC7104535/ /pubmed/32228546 http://dx.doi.org/10.1186/s12890-020-1112-3 Text en © The Author(s). 2020 Open Access This 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 Article
Wei, Sen
Liu, Jinghao
Li, Xin
Liu, Xingyu
LncRNA MIR17HG inhibits non-small cell lung cancer by upregulating miR-142-3p to downregulate Bach-1
title LncRNA MIR17HG inhibits non-small cell lung cancer by upregulating miR-142-3p to downregulate Bach-1
title_full LncRNA MIR17HG inhibits non-small cell lung cancer by upregulating miR-142-3p to downregulate Bach-1
title_fullStr LncRNA MIR17HG inhibits non-small cell lung cancer by upregulating miR-142-3p to downregulate Bach-1
title_full_unstemmed LncRNA MIR17HG inhibits non-small cell lung cancer by upregulating miR-142-3p to downregulate Bach-1
title_short LncRNA MIR17HG inhibits non-small cell lung cancer by upregulating miR-142-3p to downregulate Bach-1
title_sort lncrna mir17hg inhibits non-small cell lung cancer by upregulating mir-142-3p to downregulate bach-1
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7104535/
https://www.ncbi.nlm.nih.gov/pubmed/32228546
http://dx.doi.org/10.1186/s12890-020-1112-3
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