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Transregulation of microRNA miR-21 promoter by AP-1 transcription factor in cervical cancer cells

BACKGROUND: Gene expression profiles have demonstrated that miR-21 expression is altered in almost all types of cancers and it has been classified as an oncogenic microRNA. Persistent HPV infection is the main etiologic agent in cervical cancer and induces genetic instability, including disruption o...

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Autores principales: del Mar Díaz-González, Sacnite, Rodríguez-Aguilar, Eduardo Daniel, Meneses-Acosta, Angélica, Valadez-Graham, Viviana, Deas, Jessica, Gómez-Cerón, Claudia, Tavira-Montalván, Carlos Alberto, Arizmendi-Heras, Alitzel, Ramírez-Bello, Julián, Zurita-Ortega, Mario Enrique, Illades-Aguiar, Berenice, Leyva-Vázquez, Marco Antonio, Fernández-Tilapa, Gloria, Bermúdez-Morales, Víctor Hugo, Madrid-Marina, Vicente, Rodríguez-Dorantes, Mauricio, Pérez-Plasencia, Carlos, Peralta-Zaragoza, Oscar
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6694678/
https://www.ncbi.nlm.nih.gov/pubmed/31427899
http://dx.doi.org/10.1186/s12935-019-0931-x
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author del Mar Díaz-González, Sacnite
Rodríguez-Aguilar, Eduardo Daniel
Meneses-Acosta, Angélica
Valadez-Graham, Viviana
Deas, Jessica
Gómez-Cerón, Claudia
Tavira-Montalván, Carlos Alberto
Arizmendi-Heras, Alitzel
Ramírez-Bello, Julián
Zurita-Ortega, Mario Enrique
Illades-Aguiar, Berenice
Leyva-Vázquez, Marco Antonio
Fernández-Tilapa, Gloria
Bermúdez-Morales, Víctor Hugo
Madrid-Marina, Vicente
Rodríguez-Dorantes, Mauricio
Pérez-Plasencia, Carlos
Peralta-Zaragoza, Oscar
author_facet del Mar Díaz-González, Sacnite
Rodríguez-Aguilar, Eduardo Daniel
Meneses-Acosta, Angélica
Valadez-Graham, Viviana
Deas, Jessica
Gómez-Cerón, Claudia
Tavira-Montalván, Carlos Alberto
Arizmendi-Heras, Alitzel
Ramírez-Bello, Julián
Zurita-Ortega, Mario Enrique
Illades-Aguiar, Berenice
Leyva-Vázquez, Marco Antonio
Fernández-Tilapa, Gloria
Bermúdez-Morales, Víctor Hugo
Madrid-Marina, Vicente
Rodríguez-Dorantes, Mauricio
Pérez-Plasencia, Carlos
Peralta-Zaragoza, Oscar
author_sort del Mar Díaz-González, Sacnite
collection PubMed
description BACKGROUND: Gene expression profiles have demonstrated that miR-21 expression is altered in almost all types of cancers and it has been classified as an oncogenic microRNA. Persistent HPV infection is the main etiologic agent in cervical cancer and induces genetic instability, including disruption of microRNA gene expression. In the present study, we analyzed the underlying mechanism of how AP-1 transcription factor can active miR-21 gene expression in cervical cancer cells. METHODS: To identify that c-Fos and c-Jun regulate the expression of miR-21 we performed RT-qPCR and western blot assays. We analyzed the interaction of AP-1 with miR-21 promoter by EMSA and ChIP assays and determined the mechanism of its regulation by reporter construct plasmids. We identified the nuclear translocation of c-Fos and c-Jun by immunofluorescence microscopy assays. RESULTS: We demonstrated that c-Fos and c-Jun proteins are expressed and regulate the expression of miR-21 in cervical cancer cells. DNA sequence analysis revealed the presence of AP-1 DNA-binding sites in the human miR-21 promoter region. EMSA analyses confirmed the interactions of the miR-21 upstream transcription factor AP-1. ChIP assays further showed the binding of c-Fos to AP-1 sequences from the miR-21 core promoter in vivo. Functional analysis of AP-1 sequences of miR-21 in reporter plasmids demonstrated that these sequences increase the miR-21 promoter activation. CONCLUSIONS: Our findings suggest a physical interaction and functional cooperation between AP-1 transcription factor in the miR-21 promoter and may explain the effect of AP-1 on miR-21 gene expression in cervical cancer cells.
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spelling pubmed-66946782019-08-19 Transregulation of microRNA miR-21 promoter by AP-1 transcription factor in cervical cancer cells del Mar Díaz-González, Sacnite Rodríguez-Aguilar, Eduardo Daniel Meneses-Acosta, Angélica Valadez-Graham, Viviana Deas, Jessica Gómez-Cerón, Claudia Tavira-Montalván, Carlos Alberto Arizmendi-Heras, Alitzel Ramírez-Bello, Julián Zurita-Ortega, Mario Enrique Illades-Aguiar, Berenice Leyva-Vázquez, Marco Antonio Fernández-Tilapa, Gloria Bermúdez-Morales, Víctor Hugo Madrid-Marina, Vicente Rodríguez-Dorantes, Mauricio Pérez-Plasencia, Carlos Peralta-Zaragoza, Oscar Cancer Cell Int Primary Research BACKGROUND: Gene expression profiles have demonstrated that miR-21 expression is altered in almost all types of cancers and it has been classified as an oncogenic microRNA. Persistent HPV infection is the main etiologic agent in cervical cancer and induces genetic instability, including disruption of microRNA gene expression. In the present study, we analyzed the underlying mechanism of how AP-1 transcription factor can active miR-21 gene expression in cervical cancer cells. METHODS: To identify that c-Fos and c-Jun regulate the expression of miR-21 we performed RT-qPCR and western blot assays. We analyzed the interaction of AP-1 with miR-21 promoter by EMSA and ChIP assays and determined the mechanism of its regulation by reporter construct plasmids. We identified the nuclear translocation of c-Fos and c-Jun by immunofluorescence microscopy assays. RESULTS: We demonstrated that c-Fos and c-Jun proteins are expressed and regulate the expression of miR-21 in cervical cancer cells. DNA sequence analysis revealed the presence of AP-1 DNA-binding sites in the human miR-21 promoter region. EMSA analyses confirmed the interactions of the miR-21 upstream transcription factor AP-1. ChIP assays further showed the binding of c-Fos to AP-1 sequences from the miR-21 core promoter in vivo. Functional analysis of AP-1 sequences of miR-21 in reporter plasmids demonstrated that these sequences increase the miR-21 promoter activation. CONCLUSIONS: Our findings suggest a physical interaction and functional cooperation between AP-1 transcription factor in the miR-21 promoter and may explain the effect of AP-1 on miR-21 gene expression in cervical cancer cells. BioMed Central 2019-08-15 /pmc/articles/PMC6694678/ /pubmed/31427899 http://dx.doi.org/10.1186/s12935-019-0931-x Text en © The Author(s) 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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.
spellingShingle Primary Research
del Mar Díaz-González, Sacnite
Rodríguez-Aguilar, Eduardo Daniel
Meneses-Acosta, Angélica
Valadez-Graham, Viviana
Deas, Jessica
Gómez-Cerón, Claudia
Tavira-Montalván, Carlos Alberto
Arizmendi-Heras, Alitzel
Ramírez-Bello, Julián
Zurita-Ortega, Mario Enrique
Illades-Aguiar, Berenice
Leyva-Vázquez, Marco Antonio
Fernández-Tilapa, Gloria
Bermúdez-Morales, Víctor Hugo
Madrid-Marina, Vicente
Rodríguez-Dorantes, Mauricio
Pérez-Plasencia, Carlos
Peralta-Zaragoza, Oscar
Transregulation of microRNA miR-21 promoter by AP-1 transcription factor in cervical cancer cells
title Transregulation of microRNA miR-21 promoter by AP-1 transcription factor in cervical cancer cells
title_full Transregulation of microRNA miR-21 promoter by AP-1 transcription factor in cervical cancer cells
title_fullStr Transregulation of microRNA miR-21 promoter by AP-1 transcription factor in cervical cancer cells
title_full_unstemmed Transregulation of microRNA miR-21 promoter by AP-1 transcription factor in cervical cancer cells
title_short Transregulation of microRNA miR-21 promoter by AP-1 transcription factor in cervical cancer cells
title_sort transregulation of microrna mir-21 promoter by ap-1 transcription factor in cervical cancer cells
topic Primary Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6694678/
https://www.ncbi.nlm.nih.gov/pubmed/31427899
http://dx.doi.org/10.1186/s12935-019-0931-x
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