| http://purl.uniprot.org/citations/20160041 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/20160041 | http://www.w3.org/2000/01/rdf-schema#comment | "FOXA1 and FOXA2, members of the forkhead transcription factor family, are critical for epithelial differentiation in many endoderm-derived organs, including the pancreas. However, their role in tumor progression is largely unknown. Here, we identified FOXA1 and FOXA2 as important antagonists of the epithelial-to-mesenchymal transition (EMT) in pancreatic ductal adenocarcinoma (PDA) through their positive regulation of E-cadherin and maintenance of the epithelial phenotype. In human PDA samples, FOXA1/2 are expressed in all epithelia from normal to well-differentiated cancer cells, but are lost in undifferentiated cancer cells. In PDA cell lines, FOXA1/2 expression is consistently suppressed in experimental EMT models and RNAi silencing of FOXA1/2 alone is sufficient to induce EMT. Conversely, ectopic FOXA1/2 expression can potently neutralize several EMT-related E-cadherin repressive mechanisms. Finally, ectopic FOXA2 expression could reactivate E-cadherin expression in a PDA cell line with extensive promoter hypermethylation. In fact, demethylation-mediated reactivation of E-cadherin expression in these cells required concurrent reactivation of endogenous FOXA2 expression. We conclude that suppression of FOXA1/2 expression is both necessary and sufficient for EMT during PDA malignant progression."xsd:string |
| http://purl.uniprot.org/citations/20160041 | http://purl.org/dc/terms/identifier | "doi:10.1158/0008-5472.can-09-2979"xsd:string |
| http://purl.uniprot.org/citations/20160041 | http://purl.uniprot.org/core/author | "Song Y."xsd:string |
| http://purl.uniprot.org/citations/20160041 | http://purl.uniprot.org/core/author | "Washington M.K."xsd:string |
| http://purl.uniprot.org/citations/20160041 | http://purl.uniprot.org/core/author | "Crawford H.C."xsd:string |
| http://purl.uniprot.org/citations/20160041 | http://purl.uniprot.org/core/date | "2010"xsd:gYear |
| http://purl.uniprot.org/citations/20160041 | http://purl.uniprot.org/core/name | "Cancer Res"xsd:string |
| http://purl.uniprot.org/citations/20160041 | http://purl.uniprot.org/core/pages | "2115-2125"xsd:string |
| http://purl.uniprot.org/citations/20160041 | http://purl.uniprot.org/core/title | "Loss of FOXA1/2 is essential for the epithelial-to-mesenchymal transition in pancreatic cancer."xsd:string |
| http://purl.uniprot.org/citations/20160041 | http://purl.uniprot.org/core/volume | "70"xsd:string |
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