http://www.cnr.it/ontology/cnr/individuo/prodotto/ID27687
Sam68 regulates EMT through alternative splicing-activated nonsense-mediated mRNA decay of the SF2/ASF proto-oncogene. (Articolo in rivista)
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- Sam68 regulates EMT through alternative splicing-activated nonsense-mediated mRNA decay of the SF2/ASF proto-oncogene. (Articolo in rivista) (literal)
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- 2010-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1083/jcb.201001073 (literal)
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Valacca C; Bonomi S; Buratti E; Pedrotti S; Baralle FE; Sette C; Ghigna C; Biamonti G. (2010)
Sam68 regulates EMT through alternative splicing-activated nonsense-mediated mRNA decay of the SF2/ASF proto-oncogene.
in The Journal of cell biology; Rockefeller University Press, New York (Stati Uniti d'America)
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- Valacca C; Bonomi S; Buratti E; Pedrotti S; Baralle FE; Sette C; Ghigna C; Biamonti G. (literal)
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- Istituto di Genetica Molecolare, Consiglio Nazionale delle Ricerche (IGM-CNR), 27100 Pavia, Italy; International Centre for Genetic Engineering and Biotechnology, 34012 Trieste, Italy; Department of Public Health and Cell Biology, University of Rome Tor Vergata, 00133 Rome Italy; Laboratory of Neuroembryology, Fondazione Santa Lucia, 00143 Rome, Italy (literal)
- Titolo
- Sam68 regulates EMT through alternative splicing-activated nonsense-mediated mRNA decay of the SF2/ASF proto-oncogene. (literal)
- Abstract
- Epithelial-to-mesenchymal transition (EMT) and its reversal (MET) are crucial cell plasticity programs that act during development and tumor metastasis. We have previously shown that the splicing factor and proto-oncogene SF2/ASF impacts EMT/MET through production of a constitutively active splice variant of the Ron proto-oncogene. Using an in vitro model, we now show that SF2/ASF is also regulated during EMT/MET by alternative splicing associated with the nonsense-mediated mRNA decay pathway (AS-NMD). Overexpression and small interfering RNA experiments implicate the splicing regulator Sam68 in AS-NMD of SF2/ASF transcripts and in the choice between EMT/MET programs. Moreover, Sam68 modulation of SF2/ASF splicing appears to be controlled by epithelial cell-derived soluble factors that act through the ERK1/2 signaling pathway to regulate Sam68 phosphorylation. Collectively, our results reveal a hierarchy of splicing factors that integrate splicing decisions into EMT/MET programs in response to extracellular stimuli. (literal)
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