Analysis of copy number alterations reveals the lncRNA ALAL-1 as a regulator of lung cancer immune evasion

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dc.contributor.authorAthie, Alejandro
dc.contributor.authorMarchese, Francesco P.
dc.contributor.authorGonzález, Jovanna
dc.contributor.authorLozano, Teresa
dc.contributor.authorRaimondi, Ivan
dc.contributor.authorJuvvuna, Prasanna Kumar
dc.contributor.authorAbad, Amaya
dc.contributor.authorMarin-Béjar, Oskar
dc.contributor.authorSerizay, Jacques
dc.contributor.authorMartínez, Dannys
dc.contributor.authorAjona, Daniel
dc.contributor.authorPajares Villandiego, María Josefa
dc.contributor.authorSandoval, Juan
dc.contributor.authorMontuenga, Luis M.
dc.contributor.authorKanduri, Chandrasekhar
dc.contributor.authorLasarte, Juan José
dc.contributor.authorHuarte, Maite
dc.contributor.departmentCiencias de la Saludes_ES
dc.contributor.departmentOsasun Zientziakeu
dc.date.accessioned2025-01-27T18:06:50Z
dc.date.available2025-01-27T18:06:50Z
dc.date.issued2020
dc.date.updated2025-01-27T17:35:53Z
dc.description.abstractCancer is characterized by genomic instability leading to deletion or amplification of oncogenes or tumor suppressors. However, most of the altered regions are devoid of known cancer drivers. Here, we identify lncRNAs frequently lost or amplified in cancer. Among them, we found amplified lncRNA associated with lung cancer-1 (ALAL-1) as frequently amplified in lung adenocarcinomas. ALAL-1 is also overexpressed in additional tumor types, such as lung squamous carcinoma. The RNA product of ALAL-1 is able to promote the proliferation and tumorigenicity of lung cancer cells. ALAL-1 is a TNFα− and NF-κB–induced cytoplasmic lncRNA that specifically interacts with SART3, regulating the subcellular localization of the protein deubiquitinase USP4 and, in turn, its function in the cell. Interestingly, ALAL-1 expression inversely correlates with the immune infiltration of lung squamous tumors, while tumors with ALAL-1 amplification show lower infiltration of several types of immune cells. We have thus unveiled a pro-oncogenic lncRNA that mediates cancer immune evasion, pointing to a new target for immune potentiation.en
dc.description.sponsorshipA. Athie was supported by the Spanish Ministry of Economy Fellowship (BES-2012-055697). The research is supported by the European Research Council Starting and Consolidator grants 281877 and 771425 and by the Spanish Ministry of Economy grant BFU2014-58027-R.
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dc.format.mimetypeapplication/zipen
dc.identifier.citationAthie, A., Marchese,F.P., González, J., Lozano, T., Raimondi, I., Juvvuna, P.K., Abad, A., Marin-Bejar, O., Serizay, J., Martínez, D., Ajona, D, Pajares, M.J., Sandoval, J., Montuenga, L.M., Kanduri, C., Lasarte, J.J., Huarte, M.J. (2020) Analysis of copy number alterations reveals the lncRNA ALAL-1 as a regulator of lung cancer immune evasion. Journal of Cell Biology, 219(9), 201908078-201908078. https://doi.org/10.1083/jcb.201908078.
dc.identifier.doi10.1083/jcb.201908078
dc.identifier.issn0021-9525
dc.identifier.urihttps://academica-e.unavarra.es/handle/2454/53107
dc.language.isoeng
dc.publisherRockefeller University Press
dc.relation.ispartofJournal of Cell Biology 2020, 219(9), e201908078
dc.relation.projectIDinfo:eu-repo/grantAgreement/European Commission/Horizon 2020 Framework Programme/281877/
dc.relation.projectIDinfo:eu-repo/grantAgreement/European Commission/Horizon 2020 Framework Programme/771425/
dc.relation.projectIDinfo:eu-repo/grantAgreement/MINECO//BES-2012-055697/ES/
dc.relation.projectIDinfo:eu-repo/grantAgreement/MINECO//BFU2014-58027-R/ES/
dc.relation.publisherversionhttps://doi.org/10.1083/jcb.201908078
dc.rights© 2020 Athie et al. This article is available under a Creative Commons License Attribution 4.0 International.
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectCanceren
dc.subjectRNA biologyen
dc.subjectlncRNAen
dc.subjectALAL-1en
dc.titleAnalysis of copy number alterations reveals the lncRNA ALAL-1 as a regulator of lung cancer immune evasionen
dc.typeinfo:eu-repo/semantics/article
dc.type.versioninfo:eu-repo/semantics/publishedVersion
dspace.entity.typePublication
relation.isAuthorOfPublication601df8fd-4b6f-47c4-be5d-4b81d2c1cf64
relation.isAuthorOfPublication.latestForDiscovery601df8fd-4b6f-47c4-be5d-4b81d2c1cf64

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