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First published online March 18, 2009

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E2-2 factors in EMT

Epithelial-to-mesenchymal transition (EMT) occurs in physiological settings that involve cell migration and invasion, such as embryonic development, wound healing and cancer. Reduced expression of the cell-cell-adhesion protein E-cadherin is an indicator of EMT, and it is known that its repression can be mediated by several transcription factors (including Snail1, Snail2 and E47). On p. 1014, Amparo Cano and colleagues now show that the E-proteins E2-2A and E2-2B (which are related isoforms that are both encoded by the Tcf4 gene) can also induce EMT. They show that the overexpression of either E2-2A or E2-2B in MDCK cells leads to the acquisition of a mesenchymal phenotype and repression of E-cadherin expression. Furthermore, MDCK cells overexpressing E2-2 factors have increased migratory and invasive behaviour in vitro. However, chromatin immunoprecipitation analysis indicates that, unlike Snail1, E2-2 factors do not bind directly to the gene encoding E-cadherin, suggesting an indirect mechanism of repression. In addition, the gene-expression profile induced by the overexpression of E2-2 factors only partially overlaps with that induced by E47. Therefore, the authors conclude that the role of E2-2 factors is complementary to that of other transcription factors that repress E-cadherin transcription and induce EMT.

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The class I bHLH factors E2-2A and E2-2B regulate EMT

Verónica R. Sobrado, Gema Moreno-Bueno, Eva Cubillo, Liam J. Holt, M. Angela Nieto, Francisco Portillo, and Amparo Cano
JCS 2009 122: 1014-1024. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?