Downregulation of E-cadherin is a crucial event for epithelial to mesenchymal 
transition (EMT) in embryonic development and cancer progression. Using the 
EpFosER mammary tumour model we show that during EMT, upregulation of the 
transcriptional regulator deltaEF1 coincided with transcriptional repression of 
E-cadherin. Ectopic expression of deltaEF1 in epithelial cells was sufficient to 
downregulate E-cadherin and to induce EMT. Analysis of E-cadherin promoter 
activity and chromatin immunoprecipitation identified deltaEF1 as direct 
transcriptional repressor of E-cadherin. In human cancer cells, transcript 
levels of deltaEF1 correlated directly with the extent of E-cadherin repression 
and loss of the epithelial phenotype. The protein was enriched in nuclei of 
human cancer cells and physically associated with the E-cadherin promoter. RNA 
interference-mediated downregulation of deltaEF1 in cancer cells was sufficient 
to derepress E-cadherin expression and restore cell to cell adhesion, suggesting 
that deltaEF1 is a key player in late stage carcinogenesis.