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Publication : CELF1 is a central node in post-transcriptional regulatory programmes underlying EMT.

First Author  Chaudhury A Year  2016
Journal  Nat Commun Volume  7
Pages  13362 PubMed ID  27869122
Mgi Jnum  J:243075 Mgi Id  MGI:5907567
Doi  10.1038/ncomms13362 Citation  Chaudhury A, et al. (2016) CELF1 is a central node in post-transcriptional regulatory programmes underlying EMT. Nat Commun 7:13362
abstractText  The importance of translational regulation in tumour biology is increasingly appreciated. Here, we leverage polyribosomal profiling to prospectively define translational regulatory programs underlying epithelial-to-mesenchymal transition (EMT) in breast epithelial cells. We identify a group of ten translationally regulated drivers of EMT sharing a common GU-rich cis-element within the 3'-untranslated region (3'-UTR) of their mRNA. These cis-elements, necessary for the regulatory activity imparted by these 3'-UTRs, are directly bound by the CELF1 protein, which itself is regulated post-translationally during the EMT program. CELF1 is necessary and sufficient for both mesenchymal transition and metastatic colonization, and CELF1 protein, but not mRNA, is significantly overexpressed in human breast cancer tissues. Our data present an 11-component genetic pathway, invisible to transcriptional profiling approaches, in which the CELF1 protein functions as a central node controlling translational activation of genes driving EMT and ultimately tumour progression.
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