2024-03-28T21:27:52Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/1655272020-12-13T09:10:56Zcom_10261_134com_10261_1col_10261_387
Downregulation of Lnc-Spry1 mediates TGF-β-induced epithelial-mesenchymal transition by transcriptional and posttranscriptional regulatory mechanisms
Rodríguez-Mateo, Cristina
Torres, Belén
Gutiérrez, Gabriel
Pintor-Toro, José Antonio
Ministerio de Economía y Competitividad (España)
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.
2018-06-01T10:45:25Z
2018-06-01T10:45:25Z
2017
2018-06-01T10:45:26Z
artículo
Cell Death and Differentiation 24(5): 785-797 (2017)
http://hdl.handle.net/10261/165527
10.1038/cdd.2017.9
http://dx.doi.org/10.13039/501100003329
28186499
eng
Sí
info:eu-repo/grantAgreement/MINECO/Plan Estatal de Investigación Científica y Técnica y de Innovación 2013-2016/SAF2014-57632-P
closedAccess
Nature Publishing Group