CELF1 is a central node in post-transcriptional regulatory programmes underlying EMT View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-11-21

AUTHORS

Arindam Chaudhury, Shebna Cheema, Joseph M Fachini, Natee Kongchan, Guojun Lu, Lukas M Simon, Tao Wang, Sufeng Mao, Daniel G Rosen, Michael M Ittmann, Susan G Hilsenbeck, Chad A Shaw, Joel R Neilson

ABSTRACT

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. More... »

PAGES

13362

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/ncomms13362

    DOI

    http://dx.doi.org/10.1038/ncomms13362

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1019997442

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/27869122


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