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MicroRNA-191 targets CCAAT/enhanced binding protein β and functions as an oncogenic molecule in human non-small cell lung carcinoma cells

The aberrant expression of microRNAs (miRs) may be involved in tumor growth and progression in human non-small cell lung carcinoma (NSCLC). The present study aimed to investigate the potential roles of miR-191 in NSCLC. Western blotting and reverse transcription-quantitative polymerase chain reactio...

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Autores principales: Li, Fuliang, Wen, Jingjing, Shi, Jinsheng, Wang, Yun, Yang, Feifei, Liu, Chunying
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6601399/
https://www.ncbi.nlm.nih.gov/pubmed/31316611
http://dx.doi.org/10.3892/etm.2019.7668
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author Li, Fuliang
Wen, Jingjing
Shi, Jinsheng
Wang, Yun
Yang, Feifei
Liu, Chunying
author_facet Li, Fuliang
Wen, Jingjing
Shi, Jinsheng
Wang, Yun
Yang, Feifei
Liu, Chunying
author_sort Li, Fuliang
collection PubMed
description The aberrant expression of microRNAs (miRs) may be involved in tumor growth and progression in human non-small cell lung carcinoma (NSCLC). The present study aimed to investigate the potential roles of miR-191 in NSCLC. Western blotting and reverse transcription-quantitative polymerase chain reaction were performed to assess protein and/or mRNA levels. Scratch wound healing and transwell assays were performed to determine the NSCLC cell migration and invasion. A luciferase demonstrated that CCAAT/enhanced binding protein β (C/EBPβ) was a target of miR-191. Previously, miR-191 has been reported to act as an oncogenic player in multiple human cancers. C/EBPβ has been identified as a target gene of miR-191; however, the roles and underlying mechanisms of miR-191 associated with the regulation of tumor invasion in NSCLC remain unknown. In the present study, it was demonstrated that miR-191 expression levels were higher in human NSCLC tumors compared with in normal adjacent tissue and elevated miR-191 expression levels were closely associated with tumor node metastasis stage in patients with NSCLC. Furthermore, transfection with miR-191 mimic inhibited C/EBPβ expression at the mRNA and protein levels and promoted A549 cell migration and invasion. C/EBPβ was reported to be the direct target gene of miR-191 using a dual luciferase reporter assay. Finally, C/EBPβ siRNA can mimic the effects of miR-191. These findings indicated that miR-191 may function as an oncogene in NSCLC, at least partially due to its negative regulatory on C/EBPβ.
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spelling pubmed-66013992019-07-17 MicroRNA-191 targets CCAAT/enhanced binding protein β and functions as an oncogenic molecule in human non-small cell lung carcinoma cells Li, Fuliang Wen, Jingjing Shi, Jinsheng Wang, Yun Yang, Feifei Liu, Chunying Exp Ther Med Articles The aberrant expression of microRNAs (miRs) may be involved in tumor growth and progression in human non-small cell lung carcinoma (NSCLC). The present study aimed to investigate the potential roles of miR-191 in NSCLC. Western blotting and reverse transcription-quantitative polymerase chain reaction were performed to assess protein and/or mRNA levels. Scratch wound healing and transwell assays were performed to determine the NSCLC cell migration and invasion. A luciferase demonstrated that CCAAT/enhanced binding protein β (C/EBPβ) was a target of miR-191. Previously, miR-191 has been reported to act as an oncogenic player in multiple human cancers. C/EBPβ has been identified as a target gene of miR-191; however, the roles and underlying mechanisms of miR-191 associated with the regulation of tumor invasion in NSCLC remain unknown. In the present study, it was demonstrated that miR-191 expression levels were higher in human NSCLC tumors compared with in normal adjacent tissue and elevated miR-191 expression levels were closely associated with tumor node metastasis stage in patients with NSCLC. Furthermore, transfection with miR-191 mimic inhibited C/EBPβ expression at the mRNA and protein levels and promoted A549 cell migration and invasion. C/EBPβ was reported to be the direct target gene of miR-191 using a dual luciferase reporter assay. Finally, C/EBPβ siRNA can mimic the effects of miR-191. These findings indicated that miR-191 may function as an oncogene in NSCLC, at least partially due to its negative regulatory on C/EBPβ. D.A. Spandidos 2019-08 2019-06-13 /pmc/articles/PMC6601399/ /pubmed/31316611 http://dx.doi.org/10.3892/etm.2019.7668 Text en Copyright: © Li et al. 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
Li, Fuliang
Wen, Jingjing
Shi, Jinsheng
Wang, Yun
Yang, Feifei
Liu, Chunying
MicroRNA-191 targets CCAAT/enhanced binding protein β and functions as an oncogenic molecule in human non-small cell lung carcinoma cells
title MicroRNA-191 targets CCAAT/enhanced binding protein β and functions as an oncogenic molecule in human non-small cell lung carcinoma cells
title_full MicroRNA-191 targets CCAAT/enhanced binding protein β and functions as an oncogenic molecule in human non-small cell lung carcinoma cells
title_fullStr MicroRNA-191 targets CCAAT/enhanced binding protein β and functions as an oncogenic molecule in human non-small cell lung carcinoma cells
title_full_unstemmed MicroRNA-191 targets CCAAT/enhanced binding protein β and functions as an oncogenic molecule in human non-small cell lung carcinoma cells
title_short MicroRNA-191 targets CCAAT/enhanced binding protein β and functions as an oncogenic molecule in human non-small cell lung carcinoma cells
title_sort microrna-191 targets ccaat/enhanced binding protein β and functions as an oncogenic molecule in human non-small cell lung carcinoma cells
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6601399/
https://www.ncbi.nlm.nih.gov/pubmed/31316611
http://dx.doi.org/10.3892/etm.2019.7668
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