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dc.contributor.author | Jimenez-Garcia, Lidia | |
dc.contributor.author | Herranz, Sandra | |
dc.contributor.author | Higueras, María Angeles | |
dc.contributor.author | Luque, Alfonso | |
dc.contributor.author | Hortelano, Sonsoles | |
dc.date.accessioned | 2020-04-17T16:11:36Z | |
dc.date.available | 2020-04-17T16:11:36Z | |
dc.date.issued | 2016-10-11 | |
dc.identifier.citation | Oncotarget. 2016 Oct 11;7(41):66835-66850. d | es_ES |
dc.identifier.issn | 1949-2553 | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/9616 | |
dc.description.abstract | Tumor microenvironment has been described to play a key role in tumor growth, progression, and metastasis. Macrophages are a major cellular constituent of the tumor stroma, and particularly tumor associated macrophages (TAMs or M2-like macrophages) exert important immunosuppressive activity and a pro-tumoral role within the tumor microenvironment. Alternative-reading frame (ARF) gene is widely inactivated in human cancer. We have previously demonstrated that ARF deficiency severely impairs inflammatory response establishing a new role for ARF in the regulation of innate immunity. On the basis of these observations, we hypothesized that ARF may also regulates tumor growth through recruitment and modulation of the macrophage phenotype in the tumor microenvironment. Xenograft assays of B16F10 melanoma cells into ARF-deficient mice resulted in increased tumor growth compared to those implanted in WT control mice. Tumors from ARF-deficient mice exhibited significantly increased number of TAMs as well as microvascular density. Transwell assays showed crosstalk between tumor cells and macrophages. On the one hand, ARF-deficient macrophages modulate migratory ability of the tumor cells. And on the other, tumor cells promote the skewing of ARF-/- macrophages toward a M2-type polarization. In conclusion, these results demonstrate that ARF deficiency facilitates the infiltration of macrophages into the tumor mass and favors their polarization towards a M2 phenotype, thus promoting tumor angiogenesis and tumor growth. This work provides novel information about the critical role of ARF in the modulation of tumor microenvironment. | es_ES |
dc.description.sponsorship | This study was supported by grant PI11.0036 and PI14.0055 from the FIS, MPY 1410/09 from ISCIII and Spanish Ministry of Health (Instituto de Salud Carlos III; RD12/0036/0059) to SH, and by grant TPY-M-1068/13 and IERPY 1149/16 to AL. L J-G was supported by FIS (FI12/00340). AL was supported by FIS (CP12/03087). S Herranz was supported by TPY-M-1068/13 from ISCIII. We thank Fernando González Camacho and Silvia Hernández Esteban for Confocal Microscopy assistance. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Impact Journals | es_ES |
dc.type.hasVersion | VoR | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | * |
dc.subject | ARF | es_ES |
dc.subject | M2-polarization | es_ES |
dc.subject | angiogenesis | es_ES |
dc.subject | macrophage | es_ES |
dc.subject | tumor-microenvironment | es_ES |
dc.subject.mesh | Animals | es_ES |
dc.subject.mesh | Cell Line, Tumor | es_ES |
dc.subject.mesh | Cell Movement | es_ES |
dc.subject.mesh | Humans | es_ES |
dc.subject.mesh | Macrophage Activation | es_ES |
dc.subject.mesh | Macrophages | es_ES |
dc.subject.mesh | Melanoma, Experimental | es_ES |
dc.subject.mesh | Mice, Inbred C57BL | es_ES |
dc.subject.mesh | Mice, Knockout | es_ES |
dc.subject.mesh | Neovascularization, Pathologic | es_ES |
dc.subject.mesh | Signal Transduction | es_ES |
dc.subject.mesh | Tumor Burden | es_ES |
dc.subject.mesh | Tumor Microenvironment | es_ES |
dc.subject.mesh | Tumor Suppressor Protein p14ARF | es_ES |
dc.title | Tumor suppressor ARF regulates tissue microenvironment and tumor growth through modulation of macrophage polarization | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Atribución 4.0 Internacional | * |
dc.identifier.pubmedID | 27572316 | es_ES |
dc.format.volume | 7 | es_ES |
dc.format.number | 41 | es_ES |
dc.format.page | 66835-66850 | es_ES |
dc.identifier.doi | 10.18632/oncotarget.11652 | es_ES |
dc.contributor.funder | Instituto de Salud Carlos III | |
dc.description.peerreviewed | Sí | es_ES |
dc.identifier.e-issn | 1949-2553 | es_ES |
dc.relation.publisherversion | https://doi.org/10.18632/oncotarget.11652 | es_ES |
dc.identifier.journal | Oncotarget | es_ES |
dc.repisalud.centro | ISCIII::Instituto de Investigación de Enfermedades Raras | es_ES |
dc.repisalud.institucion | ISCIII | es_ES |
dc.relation.projectID | info:eu_repo/grantAgreement/ES/PI11.0036 | es_ES |
dc.relation.projectID | info:eu_repo/grantAgreement/ES/PI14.0055 | es_ES |
dc.relation.projectID | info:eu_repo/grantAgreement/ES/MPY 1410/09 | es_ES |
dc.relation.projectID | info:eu_repo/grantAgreement/ES/RD12/0036/0059 | es_ES |
dc.relation.projectID | info:eu_repo/grantAgreement/ES/IERPY 1149/16 | es_ES |
dc.relation.projectID | info:eu_repo/grantAgreement/ES/FI12/00340 | es_ES |
dc.relation.projectID | info:eu_repo/grantAgreement/ES/CP12/03087 | es_ES |
dc.relation.projectID | info:eu_repo/grantAgreement/ES/TPY-M-1068/13 | es_ES |
dc.rights.accessRights | open access | es_ES |