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DNA methylation data for identification of epigenetic targets of resveratrol in triple negative breast cancer cells

Previous studies revealed that some bioactive food components have anti-cancer effects. However epigenetic effects of dietary compound resveratrol are largely unknown in breast cancer cells (M.A. Dawson, T. Kouzarides, 2012) [1]. Here we provide novel data and comparisons of DNA methylation status o...

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Autores principales: Medina-Aguilar, Rubiceli, Pérez-Plasencia, Carlos, Gariglio, Patricio, Marchat, Laurence A., Flores-Pérez, Ali, López-Camarillo, César, García Mena, Jaime
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5312642/
https://www.ncbi.nlm.nih.gov/pubmed/28229117
http://dx.doi.org/10.1016/j.dib.2017.02.006
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author Medina-Aguilar, Rubiceli
Pérez-Plasencia, Carlos
Gariglio, Patricio
Marchat, Laurence A.
Flores-Pérez, Ali
López-Camarillo, César
García Mena, Jaime
author_facet Medina-Aguilar, Rubiceli
Pérez-Plasencia, Carlos
Gariglio, Patricio
Marchat, Laurence A.
Flores-Pérez, Ali
López-Camarillo, César
García Mena, Jaime
author_sort Medina-Aguilar, Rubiceli
collection PubMed
description Previous studies revealed that some bioactive food components have anti-cancer effects. However epigenetic effects of dietary compound resveratrol are largely unknown in breast cancer cells (M.A. Dawson, T. Kouzarides, 2012) [1]. Here we provide novel data and comparisons of DNA methylation status of promoter gene regions in response to resveratrol treatment at 24 h and 48 h versus untreated MDA-MB-231 breast cancer cells. DNA methylation changes were measured using Array-PRIMES method (aPRIMES) followed by whole-genome hybridization using human DNA methylation promoter microarray NimbleGen HG18 Refseq Promoter 3×720 K array. Our data were associated to corresponding changes in mRNA expression in a set of cancer-related genes. Using gene ontology analysis we also identify cancer-related cellular processes and pathways that can be epigenetically reprogramed by resveratrol. Data in this article are associated to the research articles “Methylation Landscape of Human Breast Cancer Cells in Response to Dietary Compound Resveratrol”. Medina Aguilar et al., PLoS ONE 11(6): e0157866. doi:10.1371/journal.pone.0157866 2016 (A.R. Medina, P.C. Pérez, L.A. Marchat, P. Gariglio, M.J. García, C.S. Rodríguez, G.E. Ruíz, et al., 2016) [2]; and “Resveratrol inhibits cell cycle progression by targeting Aurora kinase A and Polo-like kinase 1 in breast cancer cells” in Oncology Reports. Medina Aguilar et al., 2016 Jun; 35(6):3696-704. doi: 10.3892/or.2016.4728 (A.R. Medina, P. Gariglio, M.J. García, O.E. Arechaga, S.N. Villegas, C.M. Martínez et al., 2016) [3].
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spelling pubmed-53126422017-02-22 DNA methylation data for identification of epigenetic targets of resveratrol in triple negative breast cancer cells Medina-Aguilar, Rubiceli Pérez-Plasencia, Carlos Gariglio, Patricio Marchat, Laurence A. Flores-Pérez, Ali López-Camarillo, César García Mena, Jaime Data Brief Medicine and Dentistry Previous studies revealed that some bioactive food components have anti-cancer effects. However epigenetic effects of dietary compound resveratrol are largely unknown in breast cancer cells (M.A. Dawson, T. Kouzarides, 2012) [1]. Here we provide novel data and comparisons of DNA methylation status of promoter gene regions in response to resveratrol treatment at 24 h and 48 h versus untreated MDA-MB-231 breast cancer cells. DNA methylation changes were measured using Array-PRIMES method (aPRIMES) followed by whole-genome hybridization using human DNA methylation promoter microarray NimbleGen HG18 Refseq Promoter 3×720 K array. Our data were associated to corresponding changes in mRNA expression in a set of cancer-related genes. Using gene ontology analysis we also identify cancer-related cellular processes and pathways that can be epigenetically reprogramed by resveratrol. Data in this article are associated to the research articles “Methylation Landscape of Human Breast Cancer Cells in Response to Dietary Compound Resveratrol”. Medina Aguilar et al., PLoS ONE 11(6): e0157866. doi:10.1371/journal.pone.0157866 2016 (A.R. Medina, P.C. Pérez, L.A. Marchat, P. Gariglio, M.J. García, C.S. Rodríguez, G.E. Ruíz, et al., 2016) [2]; and “Resveratrol inhibits cell cycle progression by targeting Aurora kinase A and Polo-like kinase 1 in breast cancer cells” in Oncology Reports. Medina Aguilar et al., 2016 Jun; 35(6):3696-704. doi: 10.3892/or.2016.4728 (A.R. Medina, P. Gariglio, M.J. García, O.E. Arechaga, S.N. Villegas, C.M. Martínez et al., 2016) [3]. Elsevier 2017-02-09 /pmc/articles/PMC5312642/ /pubmed/28229117 http://dx.doi.org/10.1016/j.dib.2017.02.006 Text en © 2017 The Authors http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Medicine and Dentistry
Medina-Aguilar, Rubiceli
Pérez-Plasencia, Carlos
Gariglio, Patricio
Marchat, Laurence A.
Flores-Pérez, Ali
López-Camarillo, César
García Mena, Jaime
DNA methylation data for identification of epigenetic targets of resveratrol in triple negative breast cancer cells
title DNA methylation data for identification of epigenetic targets of resveratrol in triple negative breast cancer cells
title_full DNA methylation data for identification of epigenetic targets of resveratrol in triple negative breast cancer cells
title_fullStr DNA methylation data for identification of epigenetic targets of resveratrol in triple negative breast cancer cells
title_full_unstemmed DNA methylation data for identification of epigenetic targets of resveratrol in triple negative breast cancer cells
title_short DNA methylation data for identification of epigenetic targets of resveratrol in triple negative breast cancer cells
title_sort dna methylation data for identification of epigenetic targets of resveratrol in triple negative breast cancer cells
topic Medicine and Dentistry
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5312642/
https://www.ncbi.nlm.nih.gov/pubmed/28229117
http://dx.doi.org/10.1016/j.dib.2017.02.006
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