| First Author | Sobrado VR | Year | 2009 |
| Journal | J Cell Sci | Volume | 122 |
| Issue | Pt 7 | Pages | 1014-24 |
| PubMed ID | 19295128 | Mgi Jnum | J:150518 |
| Mgi Id | MGI:3850904 | Doi | 10.1242/jcs.028241 |
| Citation | Sobrado VR, et al. (2009) The class I bHLH factors E2-2A and E2-2B regulate EMT. J Cell Sci 122(Pt 7):1014-24 |
| abstractText | 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. |
