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dc.contributor.author | Visnes, Torkild | |
dc.contributor.author | Benítez-Buelga, Carlos | |
dc.contributor.author | Cázares-Körner, Armando | |
dc.contributor.author | Sanjiv, Kumar | |
dc.contributor.author | Hanna, Bishoy M F | |
dc.contributor.author | Mortusewicz, Oliver | |
dc.contributor.author | Rajagopal, Varshni | |
dc.contributor.author | Albers, Julian J | |
dc.contributor.author | Hagey, Daniel W | |
dc.contributor.author | Bekkhus, Tove | |
dc.contributor.author | Eshtad, Saeed | |
dc.contributor.author | Baquero, Juan Miguel | |
dc.contributor.author | Masuyer, Geoffrey | |
dc.contributor.author | Wallner, Olov | |
dc.contributor.author | Müller, Sarah | |
dc.contributor.author | Pham, Therese | |
dc.contributor.author | Göktürk, Camilla | |
dc.contributor.author | Rasti, Azita | |
dc.contributor.author | Suman, Sharda | |
dc.contributor.author | Raul, Torres-Ruiz | |
dc.contributor.author | Sarno, Antonio | |
dc.contributor.author | Wiita, Elisée | |
dc.contributor.author | Homan, Evert J | |
dc.contributor.author | Karsten, Stella | |
dc.contributor.author | Marimuthu, Karthick | |
dc.contributor.author | Michel, Maurice | |
dc.contributor.author | Koolmeister, Tobias | |
dc.contributor.author | Scobie, Martin | |
dc.contributor.author | Loseva, Olga | |
dc.contributor.author | Almlöf, Ingrid | |
dc.contributor.author | Unterlass, Judith Edda | |
dc.contributor.author | Pettke, Aleksandra | |
dc.contributor.author | Boström, Johan | |
dc.contributor.author | Pandey, Monica | |
dc.contributor.author | Gad, Helge | |
dc.contributor.author | Herr, Patrick | |
dc.contributor.author | Jemth, Ann-Sofie | |
dc.contributor.author | El Andaloussi, Samir | |
dc.contributor.author | Kalderén, Christina | |
dc.contributor.author | Rodriguez-Perales, Sandra | |
dc.contributor.author | Benítez, Javier | |
dc.contributor.author | Krokan, Hans E | |
dc.contributor.author | Altun, Mikael | |
dc.contributor.author | Stenmark, Pål | |
dc.contributor.author | Berglund, Ulrika Warpman | |
dc.contributor.author | Helleday, Thomas | |
dc.contributor.author | Rodriguez Perales, Sandra | |
dc.contributor.author | El Andaloussi, Samir | |
dc.date.accessioned | 2021-03-16T08:34:58Z | |
dc.date.available | 2021-03-16T08:34:58Z | |
dc.date.issued | 2020 | |
dc.identifier.citation | Nucleic Acids Res . 2020 ;48(21):12234-12251. | es_ES |
dc.identifier.issn | 0305-1048 | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/12279 | |
dc.description.abstract | Altered oncogene expression in cancer cells causes loss of redox homeostasis resulting in oxidative DNA damage, e.g. 8-oxoguanine (8-oxoG), repaired by base excision repair (BER). PARP1 coordinates BER and relies on the upstream 8-oxoguanine-DNA glycosylase (OGG1) to recognise and excise 8-oxoG. Here we hypothesize that OGG1 may represent an attractive target to exploit reactive oxygen species (ROS) elevation in cancer. Although OGG1 depletion is well tolerated in non-transformed cells, we report here that OGG1 depletion obstructs A3 T-cell lymphoblastic acute leukemia growth in vitro and in vivo, validating OGG1 as a potential anti-cancer target. In line with this hypothesis, we show that OGG1 inhibitors (OGG1i) target a wide range of cancer cells, with a favourable therapeutic index compared to non-transformed cells. Mechanistically, OGG1i and shRNA depletion cause S-phase DNA damage, replication stress and proliferation arrest or cell death, representing a novel mechanistic approach to target cancer. This study adds OGG1 to the list of BER factors, e.g. PARP1, as potential targets for cancer treatment. | es_ES |
dc.description.sponsorship | S.R.P.'s laboratory is partially funded by funds from the Spanish National Research and Development Plan, Instituto de Salud Carlos III and FEDER [PI17/02303 to S.R.P]; R.T.R. is supported by a fellowship from the AECC scientific foundation; J.M.B. is supported by Spanish Ministry of Education, Culture and Sport [FPU15/01978]; J.B.'s laboratory is partially funded by FEDER funds, H2020 BRIDGES project and the Spanish Network on Rare Diseases (CIBERER) [FIS PI16/00440]; Faculty of Medicine at the Norwegian University of Science and Technology and the Central Norway Regional Health Authority supports [46056921 to A.S. and H.E.K.]; Svanhild and Arne Must's Fund for Medical Research (to A.S. and H.E.K.); Norwegian Research Council (to T.V.); SIN-TEF SEP project 102020885 (to T.V.); Vinnova (to A.C.K and P.S.); the Torsten and Ragnar Soderberg Foundation (to T.H.) and the Helleday Foundation (to C.B.). Funding for open access charge and project support: European Union's Horizon 2020 research and innovation programunder the Marie Sklodowska-Curie grant agreement [722729 to A.P., B.M.F.H., T.H.]; European Research Council [ERC TAROX-695376 to T.H.]; Swedish Research Council (to T.H. and P.S.); Swedish Cancer Society (to T.H. and P.S.); Swedish Children's Cancer Foundation (to T.H.); Swedish Pain Relief Foundation (to T.H.). | es_ES |
dc.language.iso | eng | es_ES |
dc.type.hasVersion | VoR | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-sa/4.0/ | * |
dc.subject.mesh | Gene Expression Regulation, Neoplastic | es_ES |
dc.subject.mesh | Animals | es_ES |
dc.subject.mesh | Antineoplastic Agents | es_ES |
dc.subject.mesh | Cell Line, Tumor | es_ES |
dc.subject.mesh | Cell Proliferation | es_ES |
dc.subject.mesh | Colonic Neoplasms | es_ES |
dc.subject.mesh | DNA Damage | es_ES |
dc.subject.mesh | DNA Glycosylases | es_ES |
dc.subject.mesh | DNA Repair | es_ES |
dc.subject.mesh | DNA Replication | es_ES |
dc.subject.mesh | DNA, Neoplasm | es_ES |
dc.subject.mesh | Enzyme Inhibitors | es_ES |
dc.subject.mesh | Guanine | es_ES |
dc.subject.mesh | HCT116 Cells | es_ES |
dc.subject.mesh | Humans | es_ES |
dc.subject.mesh | Mice | es_ES |
dc.subject.mesh | Mice, Nude | es_ES |
dc.subject.mesh | Molecular Targeted Therapy | es_ES |
dc.subject.mesh | Oxidative Stress | es_ES |
dc.subject.mesh | Poly (ADP-Ribose) Polymerase-1 | es_ES |
dc.subject.mesh | RNA, Small Interfering | es_ES |
dc.subject.mesh | Reactive Oxygen Species | es_ES |
dc.subject.mesh | Signal Transduction | es_ES |
dc.subject.mesh | Survival Analysis | es_ES |
dc.subject.mesh | Tumor Burden | es_ES |
dc.subject.mesh | Xenograft Model Antitumor Assays | es_ES |
dc.title | Targeting OGG1 arrests cancer cell proliferation by inducing replication stress. | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Atribución-NoComercial-CompartirIgual 4.0 Internacional | * |
dc.identifier.pubmedID | 33211885 | es_ES |
dc.format.volume | 48 | es_ES |
dc.format.number | 21 | es_ES |
dc.format.page | 12234-12251 | es_ES |
dc.identifier.doi | 10.1093/nar/gkaa1048 | es_ES |
dc.contributor.funder | Instituto de Salud Carlos III | |
dc.contributor.funder | Unión Europea | |
dc.description.peerreviewed | Sí | es_ES |
dc.identifier.e-issn | 1362-4962 | es_ES |
dc.relation.publisherversion | https://doi.org/10.1093/narlgkaa1048 | es_ES |
dc.identifier.journal | Nucleic acids research | es_ES |
dc.repisalud.institucion | CNIO | es_ES |
dc.repisalud.orgCNIO | CNIO::Unidades técnicas::Unidad de Citogenética Molecular | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/GR/PI17/02303 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/FPU15/01978 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/FIS PI16/00440 | es_ES |
dc.rights.accessRights | open access | es_ES |