1. The p65 subunit of NF-κB and PARP1 assist Snail1 in activating fibronectin transcription
- Author
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Antonio García de Herreros, Raquel Batlle, Josep Baulida, Jelena Stanisavljevic, and Montserrat Porta-de-la-Riva
- Subjects
Transcriptional Activation ,Protein subunit ,Cell ,Poly (ADP-Ribose) Polymerase-1 ,Cell Line ,Mesoderm ,chemistry.chemical_compound ,Mice ,Transcription (biology) ,medicine ,Animals ,Humans ,Promoter Regions, Genetic ,Gene ,Cell Nucleus ,Extracellular Matrix Proteins ,Binding Sites ,biology ,Transcription Factor RelA ,Promoter ,NF-κB ,Cell Biology ,Molecular biology ,Fibronectins ,Fibronectin ,medicine.anatomical_structure ,chemistry ,Cell culture ,biology.protein ,Snail Family Transcription Factors ,Poly(ADP-ribose) Polymerases ,Transcription Factors - Abstract
Snail1 is a transcriptional repressor of E-cadherin that triggers epithelial–mesenchymal transition (EMT). Here, we report assisted Snail1 interaction with the promoter of a typical mesenchymal gene, fibronectin (FN1), both in epithelial cells undergoing EMT and in fibroblasts. Together with Snail1, the p65 subunit of NF-κB and PARP1 bound to the FN1 promoter. We detected nuclear interaction of these proteins and demonstrated the requirement of all three for FN1 transcription. Moreover, other genes involved in cell movement mimic FN1 expression induced by Snail1 or TGF-β1 treatment and recruit p65NF-κB and Snail1 to their promoters. The molecular cooperation between Snail1 and NF-κB in transcription activation provides a new insight into how Snail1 can modulate a variety of cell programs.
- Published
- 2012