RING1B contributes to Ewing sarcoma development by repressing the NaV1.6 sodium channel and the NF-κB pathway, independently of the fusion oncoprotein.

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dc.contributor.author	Hernández-Muñoz, Inmaculada
dc.contributor.author	Figuerola, Elisabeth
dc.contributor.author	Sanchez-Molina, Sara
dc.contributor.author	Rodriguez García, Eva
dc.contributor.author	Fernández Mariño, Ana Isabel, 1984-
dc.contributor.author	Pardo-Pastor, Carlos
dc.contributor.author	Bahamonde Santos, María Isabel, 1972-
dc.contributor.author	Fernández-Fernández, José Manuel, 1967-
dc.contributor.author	García-Domínguez, Daniel J.
dc.contributor.author	Hontecillas-Prieto, Lourdes
dc.contributor.author	Lavarino, Cinzia
dc.contributor.author	Carcaboso, Angel M.
dc.contributor.author	Torres, Carmen de
dc.contributor.author	Tirado, Oscar M.
dc.contributor.author	Alava, Enrique de
dc.contributor.author	Mora, Jaume
dc.date	2016
dc.identifier.citation	Hernandez-Muñoz I, Figuerola E, Sanchez-Molina S, Rodriguez E, Fernández-Mariño AI, Pardo-Pastor C. et al. RING1B contributes to Ewing sarcoma development by repressing the NaV1.6 sodium channel and the NF-κB pathway, independently of the fusion oncoprotein. Oncotarget. 2016 Jul 19;7(29):46283-46300. doi: 10.18632/oncotarget.10092
dc.identifier.citation	1949-2553
dc.identifier.citation	http://dx.doi.org/10.18632/oncotarget.10092
dc.identifier.uri	http://hdl.handle.net/10230/28080
dc.format	application/pdf
dc.language.iso	eng
dc.publisher	Impact Journals
dc.relation	info:eu-repo/grantAgreement/ECFP7/278742
dc.relation	info:eu-repo/grantAgreement/ECFP7/602856
dc.relation	info:eu-repo/grantAgreement/ECFP7/276998
dc.rights	© 2016 Hernandez-Muñoz et al. This is an open-access article distributed under the terms of the https://creativecommons.org/licenses/by/3.0/, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
dc.rights	https://creativecommons.org/licenses/by/3.0/
dc.rights	info:eu-repo/semantics/openAccess
dc.subject	Sarcoma -- Aspectes genètics
dc.title	RING1B contributes to Ewing sarcoma development by repressing the NaV1.6 sodium channel and the NF-κB pathway, independently of the fusion oncoprotein.
dc.type	info:eu-repo/semantics/article
dc.type	info:eu-repo/semantics/publishedVersion
dc.description.abstract	Ewing sarcoma (ES) is an aggressive tumor defined by EWSR1 gene fusions that behave as an oncogene. Here we demonstrate that RING1B is highly expressed in primary ES tumors, and its expression is independent of the fusion oncogene. RING1B-depleted ES cells display an expression profile enriched in genes functionally involved in hematological development but RING1B depletion does not induce cellular differentiation. In ES cells, RING1B directly binds the SCN8A sodium channel promoter and its depletion results in enhanced Nav1.6 expression and function. The signaling pathway most significantly modulated by RING1B is NF-κB. RING1B depletion results in enhanced p105/p50 expression, which sensitizes ES cells to apoptosis by FGFR/SHP2/STAT3 blockade. Reduced NaV1.6 function protects ES cells from apoptotic cell death by maintaining low NF-κB levels. Our findings identify RING1B as a trait of the cell-of-origin and provide a potential targetable vulnerability.
dc.description.abstract	This work was supported by the Xarxa de Bancs de Tumors de Catalunya sponsored by Pla Director d’Oncologia de Catalunya and by grants from ISCIII-FEDER (PS09/00973; RIC RD12/0042/0014, Red HERACLES), Ministerio de Economía y Competitividad (MEC) (SAF2012-31089 and SAF2015-69762-R), FEDER Funds and by the Asociación Española Contra el Cáncer (AECC). E.Á.’s lab is supported by the AECC, MECFEDER (RD12/0036/0017, PT13/0010/0056, RTC-2014- 2102-1, ISCIII Sara Borrell CD06/00001, PI12/03102, PI14/01466), the European FP7 Projects EuroSARC (FP7- HEALTH-2011-two-stage, Project 278742 EUROSARC), Euroewing (FP7-HEALTH.2013.2.4.1-1, Project 602856), Fundación Memoria de DM Solorzano Barruso, Fundación Cris contra el Cáncer, Pablo Ugarte Foundation, and Fundación M. García Estrada. O.M.T. is funded by ISCIIIFEDER (CES12/021) and the AECC. AMC is funded by the European FP7 projects (FP7/2007-2013) under a Marie Curie International Reintegration Grant (PIRG- 08- GA-2010-276998) and ISCIII-FEDER (CP13/00189). The Ewing group at the Developmental Tumor Biology Laboratory, Hospital Sant Joan de Déu, is supported by the AECC and the generous donations from Pablo Ugarte Foundation.

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