Journal
ONCOGENE
Volume 35, Issue 13, Pages 1725-1735Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2015.238
Keywords
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Funding
- National Cancer Institute [CA055536, CA154663]
- Abney Foundation
- American Heart Association Pre-doctoral Fellowship [10PRE3870024]
- National Institute of General Medicine [P30GM103331, P30GM103342, P30CA138313]
- Biorepository & Tissue Analysis Shared Resource, Hollings Cancer Center, MUSC
- Gene Targeting and Knockout Shared Resource at MUSC
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The epithelial-to-mesenchymal transition (EMT) is a cellular process that functions during embryonic development and tissue regeneration, thought to be aberrantly activated in epithelial-derived cancer and has an important role in the process of metastasis. The transforming growth factor (TGF)-beta signaling pathway is a key inducer of EMT and we have elucidated a posttranscriptional mechanism by which TGF beta modulates expression of select transcripts via the RNA-binding protein hnRNP E1 during EMT. One such transcript inhibin beta A is a member of the TGF beta superfamily. Here, we show by polysome profiling that inhibin beta A is translationally regulated by TGF beta via hnRNP E1. TGF beta treatment or knockdown of hnRNP E1 relieves silencing of the inhibin beta A transcript, resulting in increased protein expression and secreted levels of the inhibin beta A homodimer, activin A. Our data indicate that the translational upregulation of inhibin beta A enhances the migration and invasion of cells that have undergone an EMT and promotes cancer progression in vivo.
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