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dc.contributor.authorBarés Junqué, Gisel
dc.contributor.authorBeà Tàrrega, Aida
dc.contributor.authorHernández, Luís
dc.contributor.authorNavaridas Fernández de Bobadilla, Raúl
dc.contributor.authorFelip, Isidre
dc.contributor.authorMegino-Luque, Cristina
dc.contributor.authorBlasco Angulo, Natividad
dc.contributor.authorNadeu, Ferran
dc.contributor.authorCampo, Elías
dc.contributor.authorLlovera i Tomàs, Marta
dc.contributor.authorDolcet Roca, Xavier
dc.contributor.authorSanchis, Daniel
dc.date.accessioned2021-09-03T10:40:12Z
dc.date.available2021-09-03T10:40:12Z
dc.date.issued2021
dc.identifier.issn2072-6694
dc.identifier.urihttp://hdl.handle.net/10459.1/71796
dc.description.abstractEndoG influences mitochondrial DNA replication and is involved in somatic cell proliferation. Here, we investigated the effect of ENDOG/Endog expression on proliferation in different tumor models. Noteworthy, ENDOG deficiency reduced proliferation of endometrial tumor cells expressing low PTEN/high p-AKT levels, and Endog deletion blunted the growth of PTEN-deficient 3D endometrial cultures. Furthermore, ENDOG silencing reduced proliferation of follicular thyroid carcinoma and glioblastoma cell lines with high p-AKT expression. High ENDOG expression was associated with a short time to treatment in a cohort of patients with chronic lymphocytic leukemia (CLL), a B-cell lymphoid neoplasm with activation of PI3K/AKT. This clinical impact was observed in the less aggressive CLL subtype with mutated IGHV in which high ENDOG and low PTEN levels were associated with worse outcome. In summary, our results show that reducing ENDOG expression hinders growth of some tumors characterized by low PTEN activity and high p-AKT expression and that ENDOG has prognostic value for some cancer types.ca_ES
dc.description.sponsorshipThis research was funded by Ministerio de Ciencia, Innovación y Universidades, Gobierno de España, grant numbers SAF2013-44942-R and PID2019-104509RB-I00 to D.S.; grant numbers SAF2016-80157-R and PID2019-104734RB-I00 to X.D.; Fundació La Marató TV3, grant number 20153810 to D.S. G.B. holds a contract from the University of Lleida; A.B. holds a contract from Fundació La Marató TV3 and IRBLleida/Diputació de Lleida; The Spanish Ministry of Science and Innovation (MICINN) through the Instituto de Salud Carlos III (ISCIII) International Cancer Genome Consortium for Chronic Lymphocytic Leukemia (ICGC-CLL Genome Project) to E.C.. Fundació La Marato de TV3 (201920-30) to L.H. Support Groups de Recerca AGAUR 2014-SGR-795 of the Generalitat de Catalunya to E.C.ca_ES
dc.language.isoengca_ES
dc.publisherMDPIca_ES
dc.relationMINECO/PN2013-2016/SAF2013-44942-Rca_ES
dc.relationMINECO/PN2017-2020/PID2019-104509RB-I00ca_ES
dc.relationMINECO/PN2013-2016/SAF2016-80157-Rca_ES
dc.relation.isformatofReproducció del document publicat a https://doi.org/10.3390/cancers13153803ca_ES
dc.relation.ispartofCancers, 2021, vol. 13, núm. 15, 3803ca_ES
dc.rightscc-by (c) Barés et al., 2021ca_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectENDOGca_ES
dc.subjectPTENca_ES
dc.subjectAKTca_ES
dc.subjectEndometrial carcinomaca_ES
dc.subjectGlioblastomca_ES
dc.subjectChronic lymphocytic leukemiaca_ES
dc.titleENDOG Impacts on Tumor Cell Proliferation and Tumor Prognosis in the Context of PI3K/PTEN Pathway Statusca_ES
dc.typeinfo:eu-repo/semantics/articleca_ES
dc.type.versioninfo:eu-repo/semantics/publishedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessca_ES
dc.identifier.doihttps://doi.org/10.3390/cancers13153803


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