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23285117
Establishment of a TGFβ-induced post-transcriptional EMT gene signature.

PLoS One, 2012;7(12):e52624.

Hussey GS[1], Link LA, Brown AS, Howley BV, Chaudhury A, Howe PH

Affiliations

PMID: 23285117DOI: 10.1371/journal.pone.0052624

Impact factor: 3.752

Abstract
A major challenge in the clinical management of human cancers is to accurately stratify patients according to risk and likelihood of a favorable response. Stratification is confounded by significant phenotypic heterogeneity in some tumor types, often without obvious criteria for subdivision. Despite intensive transcriptional array analyses, the identity and validation of cancer specific 'signature genes' remains elusive, partially because the transcriptome does not mirror the proteome. The simplification associated with transcriptomic profiling does not take into consideration changes in the relative expression among transcripts that arise due to post-transcriptional regulatory events. We have previously shown that TGFβ post-transcriptionally regulates epithelial-mesenchymal transition (EMT) by causing increased expression of two transcripts, Dab2 and ILEI, by modulating hnRNP E1 phosphorylation. Using a genome-wide combinatorial approach involving expression profiling and RIP-Chip analysis, we have identified a cohort of translationally regulated mRNAs that are induced during TGFβ-mediated EMT. Coordinated translational regulation by hnRNP E1 constitutes a post-transcriptional regulon inhibiting the expression of related EMT-facilitating genes, thus enabling the cell to rapidly and coordinately regulate multiple EMT-facilitating genes.
MeSH terms
Animals; Base Sequence; Cluster Analysis; Epithelial-Mesenchymal Transition; Gene Expression Profiling; Gene Expression Regulation; Heterogeneous-Nuclear Ribonucleoproteins; Mice; Nucleic Acid Conformation; Protein Binding; Protein Biosynthesis; RNA Processing, Post-Transcriptional; RNA, Messenger; Reproducibility of Results; Response Elements; Transforming Growth Factor beta
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