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

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 and Joel R. Neilson ()
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Arindam Chaudhury: Baylor College of Medicine
Shebna Cheema: Baylor College of Medicine
Joseph M. Fachini: Baylor College of Medicine
Natee Kongchan: Baylor College of Medicine
Guojun Lu: Baylor College of Medicine
Lukas M. Simon: Baylor College of Medicine
Tao Wang: Lester and Sue Smith Breast Center, Baylor College of Medicine
Sufeng Mao: Lester and Sue Smith Breast Center, Baylor College of Medicine
Daniel G. Rosen: Baylor College of Medicine
Michael M. Ittmann: Baylor College of Medicine
Susan G. Hilsenbeck: Dan L. Duncan Cancer Center, Baylor College of Medicine
Chad A. Shaw: Baylor College of Medicine
Joel R. Neilson: Baylor College of Medicine

Nature Communications, 2016, vol. 7, issue 1, 1-15

Abstract: 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.

Date: 2016
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DOI: 10.1038/ncomms13362

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