Large-scale analysis of genome and transcriptome alterations in multiple tumors unveils novel cancer-relevant splicing networks

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dc.contributor.author	Sebestyén, Endre
dc.contributor.author	Singh, Babita, 1986-
dc.contributor.author	Miñana Gómez, Belén
dc.contributor.author	Pagès Pinós, Amadís
dc.contributor.author	Mateo, Francesc
dc.contributor.author	Pujana, Miguel Angel
dc.contributor.author	Valcárcel, J. (Juan)
dc.contributor.author	Eyras Jiménez, Eduardo
dc.date	2016
dc.identifier.citation	Sebestyén E, Singh B, Miñana Gómez B, Pagès Pinós A, Mateo F, Pujana MA, Valcárcel J, Eyras Jiménez E. Large-scale analysis of genome and transcriptome alterations in multiple tumors unveils novel cancer-relevant splicing networks. Genome Research. 2016; 26(6): 732-744. DOI: 10.1101/gr.199935.115
dc.identifier.citation	1088-9051
dc.identifier.citation	http://dx.doi.org/10.1101/gr.199935.115
dc.identifier.uri	http://hdl.handle.net/10230/28364
dc.description.abstract	Alternative splicing is regulated by multiple RNA-binding proteins and influences the expression of most eukaryotic genes. However, the role of this process in human disease, and particularly in cancer, is only starting to be unveiled. We systematically analyzed mutation, copy number, and gene expression patterns of 1348 RNA-binding protein (RBP) genes in 11 solid tumor types, together with alternative splicing changes in these tumors and the enrichment of binding motifs in the alternatively spliced sequences. Our comprehensive study reveals widespread alterations in the expression of RBP genes, as well as novel mutations and copy number variations in association with multiple alternative splicing changes in cancer drivers and oncogenic pathways. Remarkably, the altered splicing patterns in several tumor types recapitulate those of undifferentiated cells. These patterns are predicted to be mainly controlled by MBNL1 and involve multiple cancer drivers, including the mitotic gene NUMA1. We show that NUMA1 alternative splicing induces enhanced cell proliferation and centrosome amplification in nontumorigenic mammary epithelial cells. Our study uncovers novel splicing networks that potentially contribute to cancer development and progression.
dc.description.abstract	We thank P. Papasaikas, B. Blencowe, M. Irimia, and Q. Morris for comments and discussions. E.S., B.S., A.P., and E.E. were supported by the Ministerio de Economía y Competitividad (MINECO) and European Commission (FEDER) (BIO2014-52566-R), Consolider RNAREG (CSD2009-00080), by Agència de Gestió d’Ajuts Universitaris i de Recerca (AGAUR) (SGR2014-1121), and by the Sandra Ibarra Foundation for Cancer (FSI2013). J.V. and B.M. were supported by Fundación Botín, by Banco de Santander through its Santander Universities Global Division, and by Consolider RNAREG (CSD2009-00080), MINECO, and AGAUR. F.M. and M.A.P. were supported by AECC (Hereditary Cancer), AGAUR (SGR2014-364), the Instituto de Salud Carlos III (ISCIII), the MINECO, and FEDER (PIE13/00022-ONCOPROFILE, PI15/00854, and RTICC RD12/0036/0008).
dc.format	application/pdf
dc.language.iso	eng
dc.publisher	Cold Spring Harbor Laboratory Press (CSHL Press)
dc.relation	Genome Research. 2016; 26(6): 732-744
dc.relation	info:eu-repo/grantAgreement/ES/3PN/CSD2009-00080
dc.rights	info:eu-repo/semantics/openAccess
dc.rights	© 2016 Sebestyén et al.; Published by Cold Spring Harbor Laboratory Press. This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genome.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.
dc.rights	http://creativecommons.org/licenses/by-nc/4.0/
dc.title	Large-scale analysis of genome and transcriptome alterations in multiple tumors unveils novel cancer-relevant splicing networks
dc.type	info:eu-repo/semantics/article
dc.type	info:eu-repo/semantics/publishedVersion

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