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Open Access item The class I bHLH factors E2-2A and E2-2B regulate EMT
|Authors:||Sobrado, Verónica R.|
Holt, Liam J.
Nieto, M. Ángela
|Keywords:||Bhlh E2-2, E-cadherin repression, Emt, E47, Snail, Tumour progression, Gene profiling|
|Publisher:||Company of Biologists|
|Citation:||Journal of Cell Science 122(7): 1014-1024 (2009)|
|Abstract:||Functional loss of the cell-cell adhesion molecule E-cadherin is an essential event for epithelial-mesenchymal transition (EMT), a process that allows cell migration during embryonic development and tumour invasion. In most carcinomas, transcriptional repression has emerged as the main mechanism responsible for E-cadherin downregulation. Here, we report the identification of class I bHLH factor E2-2 (TCF4/ITF2) as a new EMT regulator. Both isoforms of E2-2 (E2-2A and E2-2B) induce a full EMT when overexpressed in MDCK cells but without affecting the tumorigenic properties of parental cells, in contrast to other EMT inducers, such as Snail1 or class I bHLH E47. E-cadherin repression mediated by E2-2 is indirect and independent of proximal E-boxes of the promoter. Knockdown studies indicate that E2-2 expression is dispensable for maintenance of the EMT driven by Snail1 and E47. Comparative gene-profiling analysis reveals that E2-2 factors induce similar, yet distinct, genetic programs to that induced by E47 in MDCK cells. These results, together with the embryonic expression pattern of Tcf4 and E2A (which encodes E12/E47), support a distinct role for E2-2 and suggest an interesting interplay between E-cadherin repressors in the regulation of physiological and pathological EMT processes.|
|Description:||11 pages, 6 figures.|
|Publisher version (URL):||http://dx.doi.org/10.1242/jcs.028241|
|Appears in Collections:||(IIBM) Artículos|
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