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Título : MicroRNA-200 family modulation in distinct breast cancer phenotypes.
Autor : Castilla, María Ángeles
Díaz-Martín, Juan
Sarrió, David
Romero-Pérez, Laura
López-García, María Ángeles
Vieites, Begoña
Biscuola, Michele
Ramiro-Fuentes, Susana
Isacke, Clare M
Palacios, José
Filiación: [Castilla,MÁ; Díaz-Martín,J; Romero-Pérez,L; López-García,MÁ; Vieites,B; Biscuola,M; Ramiro-Fuentes,S] Instituto de Biomedicina de Sevilla-CSIC-Universidad de Sevilla, Hospital Universitario Virgen del Rocío, Department of Pathology, Seville, Spain. [Isacke,CM] Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research, London, United Kingdom. [Palacios,J] Hospital Universitario Ramón y Cajal, Department of Pathology, Madrid, Spain
Palabras clave : Neoplasias de la Mama;Fenotipo;Transición Epitelial-Mesenquimal
MeSH: Medical Subject Headings::Diseases::Neoplasms::Neoplasms by Site::Breast Neoplasms
Medical Subject Headings::Phenomena and Processes::Genetic Phenomena::Phenotype
Medical Subject Headings::Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Transdifferentiation::Epithelial-Mesenchymal Transition
Fecha de publicación : 24-oct-2012
Editorial : Public Library of Science
Cita Bibliográfica: Castilla MÁ, Díaz-Martín J, Sarrió D, Romero-Pérez L, López-García MÁ, Vieites B, et al. MicroRNA-200 family modulation in distinct breast cancer phenotypes. PLoS ONE; 7(10):e47709
Abstract: The epithelial to mesenchymal transition (EMT) contributes to tumor invasion and metastasis in a variety of cancer types. In human breast cancer, gene expression studies have determined that basal-B/claudin-low and metaplastic cancers exhibit EMT-related characteristics, but the molecular mechanisms underlying this observation are unknown. As the family of miR-200 microRNAs has been shown to regulate EMT in normal tissues and cancer, here we evaluated whether the expression of the miR-200 family (miR-200f) and their epigenetic state correlate with EMT features in human breast carcinomas. We analyzed by qRT-PCR the expression of miR-200f members and various EMT-transcriptional inducers in a series of 70 breast cancers comprising an array of phenotypic subtypes: estrogen receptor positive (ER+), HER2 positive (HER2+), and triple negative (TN), including a subset of metaplastic breast carcinomas (MBCs) with sarcomatous (homologous or heterologous) differentiation. No MBCs with squamous differentiation were included. The DNA methylation status of miR-200f loci in tumor samples were inspected using Sequenom MassArray® MALDI-TOF platform. We also used two non-tumorigenic breast basal cell lines that spontaneously undergo EMT to study the modulation of miR-200f expression during EMT in vitro. We demonstrate that miR-200f is strongly decreased in MBCs compared with other cancer types. TN and HER2+ breast cancers also exhibited lower miR-200f expression than ER+ tumors. Significantly, the decreased miR-200f expression found in MBCs is accompanied by an increase in the expression levels of EMT-transcriptional inducers, and hypermethylation of the miR-200c-141 locus. Similar to tumor samples, we demonstrated that downregulation of miR-200f and hypermethylation of the miR-200c-141 locus, together with upregulation of EMT-transcriptional inducers also occur in an in vitro cellular model of spontaneous EMT. Thus, the expression and methylation status of miR-200f could be used as hypothetical biomarkers to assess the occurrence of EMT in breast cancer.
Descripción : Journal Article; Research Support, Non-U.S. Gov't;
URI: http://hdl.handle.net/10668/847
Versión del editor : http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0047709
DOI: 10.1371/journal.pone.0047709
ISSN : 1932-6203 (Online)
Aparece en las colecciones: 01- Artículos - Hospital Virgen del Rocío
01- Artículos - IBIS. Instituto de Biomedicina de Sevilla

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