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Título

E47 and Id1 interplay in epithelial-mesenchymal transition

AutorCubillo, Eva ; Díaz-Lopez, Antonio; Cuevas, Eva P.; Moreno-Bueno, Gema ; Peinado, Héctor; Montes, Amalia; Santos, Vanesa ; Portillo, Francisco ; Cano, Amparo
Fecha de publicación2013
EditorPublic Library of Science
CitaciónPLoS ONE 8(3): e59948 (2013)
ResumenE12/E47 proteins (encoded by E2A gene) are members of the class I basic helix-loop-helix (bHLH) transcription factors (also known as E proteins). E47 has been described as repressor of E-cadherin and inducer of epithelial-mesenchymal transition (EMT). We reported previously that EMT mediated by E47 in MDCK cells occurs with a concomitant overexpression of Id1 and Id3 proteins. Id proteins belong to class V of HLH factors that lack the basic domain; they dimerise with E proteins and prevent their DNA interaction, thus, acting as dominant negative of E proteins. Here, we show that E47 interacts with Id1 in E47 overexpressing MDCK cells that underwent a full EMT as well as in mesenchymal breast carcinoma and melanoma cell lines. By conducting chromatin immunoprecipitation assays we demonstrate that E47 binds directly to the endogenous E-cadherin promoter of mesenchymal MDCK-E47 cells in a complex devoid of Id1. Importantly, our data suggest that both E47 and Id1 are required to maintain the mesenchymal phenotype of MDCK-E47 cells. These data support the collaboration between E47 and Id1 in the maintenance of EMT by mechanisms independent of the dominant negative action of Id1 on E47 binding to E-cadherin promoter. Finally, the analysis of several N0 breast tumour series indicates that the expression of E47 and ID1 is significantly associated with the basal-like phenotype supporting the biological significance of the present findings.
DescripciónThis is an open-access article distributed under the terms of the Creative Commons Attribution License.
Versión del editorhttp://dx.doi.org/10.1371/journal.pone.0059948
URIhttp://hdl.handle.net/10261/123899
DOI10.1371/journal.pone.0059948
Identificadoresdoi: 10.1371/journal.pone.0059948
issn: 1932-6203
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