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Signaling Pathways Driving Aberrant Splicing in Cancer Cells

2018-01Journal article Open access
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dc.contributor.authorGonçalves, Vânia
dc.contributor.authorPereira, Joana
dc.contributor.authorJordan, Peter
dc.date.accessioned2019-02-13T16:50:32Z
dc.date.available2019-02-13T16:50:32Z
dc.date.issued2018-01
dc.descriptionFree PMC Article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5793162/pt_PT
dc.description.abstractAberrant profiles of pre-mRNA splicing are frequently observed in cancer. At the molecular level, an altered profile results from a complex interplay between chromatin modifications, the transcriptional elongation rate of RNA polymerase, and effective binding of the spliceosome to the generated transcripts. Key players in this interplay are regulatory splicing factors (SFs) that bind to gene-specific splice-regulatory sequence elements. Although mutations in genes of some SFs were described, a major driver of aberrant splicing profiles is oncogenic signal transduction pathways. Signaling can affect either the transcriptional expression levels of SFs or the post-translational modification of SF proteins, and both modulate the ratio of nuclear versus cytoplasmic SFs in a given cell. Here, we will review currently known mechanisms by which cancer cell signaling, including the mitogen-activated protein kinases (MAPK), phosphatidylinositol 3 (PI3)-kinase pathway (PI3K) and wingless (Wnt) pathways but also signals from the tumor microenvironment, modulate the activity or subcellular localization of the Ser/Arg rich (SR) proteins and heterogeneous nuclear ribonucleoproteins (hnRNPs) families of SFs.pt_PT
dc.description.sponsorshipWork in the authors’ laboratory was supported by Fundação para a Ciência e Tecnologia (FCT) [plurianual grant UID/MULTI/04046/2013 to the research unit BioISI and fellowship SFRH/BD/109162/2015 to JFSP] and by the Portuguese association Maratona da Saúde - Cancro 2014 to PJ.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationGenes. 2018;9(1):pii: E9. Epub 2017 Dez 29. doi: 10.3390/genes9010009pt_PT
dc.identifier.doi10.3390/genes9010009pt_PT
dc.identifier.issn2073-4425
dc.identifier.urihttp://hdl.handle.net/10400.18/5798
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherMDPIpt_PT
dc.relation.publisherversionhttps://www.mdpi.com/2073-4425/9/1/9pt_PT
dc.subjectCancer Cellpt_PT
dc.subjectAlternative Splicingpt_PT
dc.subjectSignal Transductionpt_PT
dc.subjectGenetic Programpt_PT
dc.subjectSignaling Pathwaypt_PT
dc.subjectTumorigenesispt_PT
dc.subjectTumor Microenvironmentpt_PT
dc.subjectVias de Transdução de Sinal e Patologias Associadaspt_PT
dc.titleSignaling Pathways Driving Aberrant Splicing in Cancer Cellspt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/5876/UID%2FMulti%2F04046%2F2013/PT
oaire.awardURIinfo:eu-repo/grantAgreement/WT/Genetic & Molecular Sciences/109162
oaire.citation.issue1pt_PT
oaire.citation.startPagepii: E9pt_PT
oaire.citation.titleGenespt_PT
oaire.citation.volume9pt_PT
oaire.fundingStream5876
oaire.fundingStreamGenetic & Molecular Sciences
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/100010269
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameWellcome Trust
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isProjectOfPublicationdc84f768-e6f2-4eea-b294-6c8ebbd1a156
relation.isProjectOfPublication540185ab-214e-4848-8df9-1490caeacb8c
relation.isProjectOfPublication.latestForDiscoverydc84f768-e6f2-4eea-b294-6c8ebbd1a156

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