E47 and Id1 interplay in epithelial-mesenchymal transition
Entity
UAM. Departamento de BioquímicaPublisher
Public Library of ScienceDate
2013-03-26Citation
10.1371/journal.pone.0059948
Plos One 8.3 (2013): e59948
ISSN
1932-6203 (online)DOI
10.1371/journal.pone.0059948Funded by
This work was supported by the Spanish Ministry of Education and Science (SAF2007-63051; SAF2010-21143; Consolider Ingenio 2010 CDS07/00017) to A.C.; (SAF2007-63075 and SAF2010-20175) to G.M.B.; Comunidad de Madrid (S2010/BMD-2303) to A.C and G.M.BProject
Comunidad de Madrid. S2010/BMD-2303/RECARESubjects
Apoptosis; Gene Expression Regulation; Breast Neoplasms; Melanoma; Madin Darby Canine Kidney Cells; Cell Line, Tumor; MedicinaRights
© 2013 Cubillo et al.Abstract
E12/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
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Google Scholar:Cubillo, Eva
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Díaz-López, Antonio
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Cuevas, Eva P.
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Moreno Bueno, Gema
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Peinado, Hector
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Montes, Amalia
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Santos, Vanesa
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Portillo Pérez, Francisco
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Cano, Amparo
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