SIP1/ZEB2 induces EMT by repressing genes of different epithelial cell–cell junctions
作者： Cindy Vandewalle , Joke Comijn , Bram De Craene , Petra Vermassen , Erik Bruyneel
DOI: 10.1093/NAR/GKI965
关键词: Chromatin 、 Cell junction 、 Molecular biology 、 Psychological repression 、 Transcription factor 、 Cell biology 、 Biology 、 Tight junction 、 Cadherin 、 Chromatin immunoprecipitation 、 Repressor
摘要: SIP1/ZEB2 is a member of the δEF-1 family two-handed zinc finger nuclear factors. The expression these transcription factors associated with epithelial mesenchymal transitions (EMT) during development. SIP1 also expressed in some breast cancer cell lines and was detected intestinal gastric carcinomas, where its inversely correlated that E-cadherin. Here, we show human cells results clear morphological change from an to phenotype. Induction this dedifferentiation accompanied by repression several junctional proteins, concomitant their mRNA levels. Besides E-cadherin, other genes coding for crucial proteins tight junctions, desmosomes gap junctions were found be transcriptionally regulated transcriptional repressor SIP1. Moreover, study promoter regions selected luciferase reporter assays chromatin immunoprecipitation shows directly mediated These data indicate that, dedifferentiation, represses coordinated manner contributing dedifferentiated state; occurs general mechanism Smad Interacting Protein 1 (SIP1)-binding sites.
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