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DIS3L2: Unveiling a New Player in Tumorigenesis, with a Key Role in Colorectal Cancer

2023Periodical Open access
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dc.contributor.authorGarcía-Moreno, Juan F.
dc.contributor.authorMatos, Paulo
dc.contributor.authorRomão, Luísa
dc.date.accessioned2024-01-12T15:02:55Z
dc.date.available2024-01-12T15:02:55Z
dc.date.issued2023
dc.description.abstractDIS3L2 is a 3’-5’ exoribonuclease that recognizes and degrades uridylated transcripts in an exosome-independent manner and participates in several RNA degradation pathways, such as the nonsense-mediated mRNA decay, or the surveillance of aberrant structured non-coding RNAs. Although some studies have linked DIS3L2 to tumorigenesis and cancer-related processes, its exact role in the development and progression of cancer has remained unclear since the discovery of DIS3L2's ribonuclease activity a decade ago. While some authors have reported evidence of a tumor suppressor role for this exoribonuclease, other studies have shown DIS3L2 as a driver of tumorigenesis. Although differences in tissue type and methodologic approaches may somewhat account for the opposing findings, a recent study from our group further supports a pro-tumorigenic role for DIS3L2, this time in promoting colorectal cancer (CRC) progression. Indeed, proper DIS3L2 expression was proven essential to maintain key tumorigenic properties in CRC cells, including cell proliferation and invasion. Here, we summarize the current state of knowledge regarding the impact of DIS3L2 in cancer, namely in colorectal cancer. The collected data unveils DIS3L2 as a novel putative therapeutic target in cancer that warrants further investigation.pt_PT
dc.description.sponsorshipThis work was supported by Instituto Nacional de Saúde Doutor Ricardo Jorge and Fundação para a Ciência e a Tecnologia (FCT) [UID/MULTI/04046/2019 Research Unit Grant (to BioISI)]. Juan F. García-Moreno was recipient of a fellowship from BioSys PhD programme (PD/BD/142898/2018)pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationJ Cell Signal. 2023;4(4):169-177. doi:10.33696/Signaling.4.104pt_PT
dc.identifier.doi10.33696/Signaling.4.104pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.18/8897
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherScientific Archivespt_PT
dc.relationBiosystems and Integrative Sciences Institute
dc.relationThe involvement od DIS3L2 in nonsense-mediated mRNA decay and its functional networks in colorectal cancer
dc.relation.publisherversionhttps://www.scientificarchives.com/article/dis3l2-unveiling-a-new-player-in-tumorigenesis-with-a-key-role-in-colorectal-cancerpt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectDIS3L2pt_PT
dc.subjectColorectal Cancerpt_PT
dc.subjectUridylationpt_PT
dc.subjectAZGP1pt_PT
dc.subjectmTORpt_PT
dc.subjectCell Viabilitypt_PT
dc.subjectCell Migrationpt_PT
dc.subjectCell Invasionpt_PT
dc.subjectGenómica Funcionalpt_PT
dc.subjectExpressão génicapt_PT
dc.subjectGenómica Funcional e Estruturalpt_PT
dc.titleDIS3L2: Unveiling a New Player in Tumorigenesis, with a Key Role in Colorectal Cancerpt_PT
dc.typeperiodical
dspace.entity.typePublication
oaire.awardTitleBiosystems and Integrative Sciences Institute
oaire.awardTitleThe involvement od DIS3L2 in nonsense-mediated mRNA decay and its functional networks in colorectal cancer
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/6817 - DCRRNI ID/UIDB%2F04046%2F2020/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//PD%2FBD%2F142898%2F2018/PT
oaire.citation.endPage177pt_PT
oaire.citation.issue4pt_PT
oaire.citation.startPage169pt_PT
oaire.citation.titleJournal of Cellular Signalingpt_PT
oaire.citation.volume4pt_PT
oaire.fundingStream6817 - DCRRNI ID
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.embargofctAcesso de acordo com página web do editor da revista.pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typecontributionToPeriodicalpt_PT
relation.isProjectOfPublicationdc433369-36fd-4935-bd52-c56aa49c72e1
relation.isProjectOfPublicationc93cb40d-1352-4e28-985e-32ceb76f0895
relation.isProjectOfPublication.latestForDiscoverydc433369-36fd-4935-bd52-c56aa49c72e1

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