| First Author | Rodríguez-Mateo C | Year | 2017 |
| Journal | Cell Death Differ | Volume | 24 |
| Issue | 5 | Pages | 785-797 |
| PubMed ID | 28186499 | Mgi Jnum | J:268228 |
| Mgi Id | MGI:6269623 | Doi | 10.1038/cdd.2017.9 |
| Citation | Rodriguez-Mateo C, et al. (2017) Downregulation of Lnc-Spry1 mediates TGF-beta-induced epithelial-mesenchymal transition by transcriptional and posttranscriptional regulatory mechanisms. Cell Death Differ 24(5):785-797 |
| abstractText | 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-beta-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-beta. 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-beta-regulated gene targets. Moreover, lnc-Spry1 associates with U2AF65 splicing factor, suggesting a role in alternative splicing. Depletion of lnc-Spry1 induces, as TGF-beta, 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-beta signaling and reveal different roles for a lncRNA in modulating transcriptional and posttranscriptional gene expression. |
