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Title: Downregulation of Lnc-Spry1 mediates TGF-β-induced epithelial-mesenchymal transition by transcriptional and posttranscriptional regulatory mechanisms.
Authors: Rodríguez-Mateo, Cristina
Torres, Belén
Gutiérrez, Gabriel
Pintor-Toro, José A
metadata.dc.subject.mesh: Adaptor Proteins, Signal Transducing
Cell Line
Cell Movement
Cell Proliferation
Epithelial Cells
Epithelial-Mesenchymal Transition
Fibroblast Growth Factor 2
Mammary Glands, Animal
Membrane Proteins
Mice, Inbred C57BL
RNA Processing, Post-Transcriptional
RNA, Long Noncoding
Receptors, Fibroblast Growth Factor
Signal Transduction
Splicing Factor U2AF
Transcription, Genetic
Transforming Growth Factor beta
Issue Date: 10-Feb-2017
Abstract: Long non-coding RNAs (lncRNAs) are a class of regulatory genes that participate in a wide range of biological processes, including proliferation, differentiation and development, as well as in a broad spectrum of diseases. Although the role of lncRNAs in TGF-β-induced epithelial-to-mesenchymal transition (EMT) has been well established, little is known about the role of lncRNAs as immediate-early regulators of EMT. Here lnc-Spry1 is identified as an immediate-early regulator of EMT that is downregulated by TGF-β. It is also found that knockdown of lnc-Spry1 promotes a mesenchymal-like phenotype and results in increased cell migration and invasion. In addition, it is shown that lnc-Spry1 depletion preferentially affects the expression of TGF-β-regulated gene targets. Moreover, lnc-Spry1 associates with U2AF65 splicing factor, suggesting a role in alternative splicing. Depletion of lnc-Spry1 induces, as TGF-β, isoform switching of fibroblast growth factor receptors, resulting in FGF-2-sensitive cells. Taken together, these results show that lnc-Spry1 could act as an early mediator of TGF-β signaling and reveal different roles for a lncRNA in modulating transcriptional and posttranscriptional gene expression.
metadata.dc.identifier.doi: 10.1038/cdd.2017.9
Appears in Collections:Producción 2020

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