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dc.contributor.author | García-Colmenero, Lidia |
dc.contributor.author | González Miranda, Jessica |
dc.contributor.author | Sandoval, Juan |
dc.contributor.author | Guillén, Yolanda |
dc.contributor.author | Diaz-Lagares, Angel |
dc.contributor.author | Andrades, Evelyn |
dc.contributor.author | Iglesias, Arnau |
dc.contributor.author | Nonell Mazelón, Lara |
dc.contributor.author | Pujol Vallverdú, Ramon Maria |
dc.contributor.author | Bigas Salvans, Anna |
dc.contributor.author | Espinosa Blay, Lluís |
dc.contributor.author | Gallardo Hernández, Fernando |
dc.date.accessioned | 2021-06-10T07:06:24Z |
dc.date.available | 2021-06-10T07:06:24Z |
dc.date.issued | 2020 |
dc.identifier.citation | García-Colmenero L, González J, Sandoval J, Guillén Y, Diaz-Lagares A, Andrades E, et al. Epigenetic silencing of tumor suppressor miR-124 directly supports STAT3 activation in cutaneous T-Cell lymphoma. Cells. 2020 Dec 15; 9(12): 2692. DOI: 10.3390/cells9122692 |
dc.identifier.issn | 2073-4409 |
dc.identifier.uri | http://hdl.handle.net/10230/47825 |
dc.description.abstract | Increasing evidence supports a potential role for STAT3 as a tumor driver in cutaneous T-cell lymphomas (CTCL). The mechanisms leading to STAT3 activation are not fully understood; however, we recently found that miR-124, a known STAT3 regulator, is robustly silenced in MF tumor-stage and CTCL cells. Objective: We studied here whether deregulation of miR-124 contributes to STAT3 pathway activation in CTCL. Methods: We measured the effect of ectopic mir-124 expression in active phosphorylated STAT3 (p-STAT3) levels and evaluated the transcriptional impact of miR-124-dependent STAT3 pathway regulation by expression microarray analysis. Results: We found that ectopic expression of miR-124 results in massive downregulation of activated STAT3 in different CTCL lines, which resulted in a significant alteration of genetic signatures related with gene transcription and proliferation such as MYC and E2F. Conclusions: Our study highlights the importance of the miR-124/STAT3 axis in CTCL and demonstrates that the STAT3 pathway is regulated through epigenetic mechanisms in these cells. Since deregulated STAT3 signaling has a major impact on CTCL initiation and progression, a better understanding of the molecular basis of the miR-124/STAT3 axis may provide useful information for future personalized therapies. |
dc.format.mimetype | application/pdf |
dc.language.iso | eng |
dc.publisher | MDPI |
dc.rights | Copyright © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ |
dc.title | Epigenetic silencing of tumor suppressor miR-124 directly supports STAT3 activation in cutaneous T-Cell lymphoma |
dc.type | info:eu-repo/semantics/article |
dc.identifier.doi | http://dx.doi.org/10.3390/cells9122692 |
dc.subject.keyword | JAK/STAT (janus kinase/signal transducer and activator of transcription) |
dc.subject.keyword | STAT3 (signal transducer and activator of transcription-3) |
dc.subject.keyword | Sézary syndrome |
dc.subject.keyword | utaneous T-cell lymphoma |
dc.subject.keyword | miR-124 |
dc.subject.keyword | Mycosis fungoides |
dc.rights.accessRights | info:eu-repo/semantics/openAccess |
dc.type.version | info:eu-repo/semantics/publishedVersion |