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dc.creatorGuo, Feifeies
dc.creatorEstévez-Vázquez, Estheres
dc.creatorBenedé-Ubieto, Raqueles
dc.creatorAmpuero Herrojo, Javieres
dc.creatorRomero Gómez, Manueles
dc.creatorNevzorova, Yulia A.es
dc.date.accessioned2022-03-28T15:48:50Z
dc.date.available2022-03-28T15:48:50Z
dc.date.issued2021-12-31
dc.identifier.citationGuo, F., Estévez-Vázquez, E., Benedé-Ubieto, R., Ampuero Herrojo, J., Romero Gómez, M. y Nevzorova, Y.A. (2021). A Shortcut from Metabolic-Associated Fatty Liver Disease (MAFLD) to Hepatocellular Carcinoma (HCC): c-MYC a Promising Target for Preventative Strategies and Individualized Therapy. Cancers, 14 (1)
dc.identifier.issn2072-6694es
dc.identifier.urihttps://hdl.handle.net/11441/131367
dc.description.abstractBackground: Metabolic-associated fatty liver disease (MAFLD) has risen as one of the leading etiologies for hepatocellular carcinoma (HCC). Oncogenes have been suggested to be responsible for the high risk of MAFLD-related HCC. We analyzed the impact of the proto-oncogene c-MYC in the development of human and murine MAFLD and MAFLD-associated HCC. Methods: alb-myctg mice were studied at baseline conditions and after administration of Western diet (WD) in comparison to WT littermates. c-MYC expression was analyzed in biopsies of patients with MAFLD and MAFLD-associated HCC by immunohistochemistry. Results: Mild obesity, spontaneous hyperlipidaemia, glucose intolerance and insulin resistance were characteristic of 36-week-old alb-myctg mice. Middle-aged alb-myctg exhibited liver steatosis and increased triglyceride content. Liver injury and inflammation were associated with elevated ALT, an upregulation of ER-stress response and increased ROS production, collagen deposition and compensatory proliferation. At 52 weeks, 20% of transgenic mice developed HCC. WD feeding exacerbated metabolic abnormalities, steatohepatitis, fibrogenesis and tumor prevalence. Therapeutic use of metformin partly attenuated the spontaneous MAFLD phenotype of alb-myctg mice. Importantly, upregulation and nuclear localization of c-MYC were characteristic of patients with MAFLD and MAFLD-related HCC. Conclusions: A novel function of c-MYC in MAFLD progression was identified opening new avenues for preventative strategieses
dc.description.sponsorshipMINECO Retos SAF2016-78711es
dc.description.sponsorshipSAF2017-87919-Res
dc.description.sponsorshipPID2020-117827RB-IOOes
dc.description.sponsorshipPID2020-117941RB-IOOes
dc.description.sponsorshipPID2020-117116RB-I00es
dc.description.sponsorshipEXOHEP-CM S2017/BMD- 3727es
dc.description.sponsorshipNanoLiver-CM Y2018/NMT-4949es
dc.description.sponsorshipAMMF 2018/117es
dc.description.sponsorshipCOST Action CA17112es
dc.description.sponsorshipUCM-25/2019es
dc.description.sponsorshipLa Caixa Foundation Program HR17-00601es
dc.description.sponsorshipAsociación Española Contra el Cáncer AECC PROYE20084 REGUes
dc.description.sponsorshipthe German Research Foundation SFB1382 Project ID 403224013/A02es
dc.description.sponsorshipRamón y Cajal Researchers RYC-2014-15242es
dc.description.sponsorshipRYC-2015-17438es
dc.description.sponsorshipInstituto de Salud Carlos III PI16/01842, PI19/01404; PI19/00589es
dc.description.sponsorshipThe German Research Foundation SFB1382 Project ID 403224013/B07es
dc.formatapplication/pdfes
dc.format.extent19 p.es
dc.language.isoenges
dc.relation.ispartofCancers, 14 (1)
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectMetabolic-associated fatty liver disease (MAFLD)es
dc.subjectC-myces
dc.subjectOncogenees
dc.subjectTumorigenesises
dc.subjectMetformines
dc.titleA Shortcut from Metabolic-Associated Fatty Liver Disease (MAFLD) to Hepatocellular Carcinoma (HCC): c-MYC a Promising Target for Preventative Strategies and Individualized Therapyes
dc.typeinfo:eu-repo/semantics/articlees
dcterms.identifierhttps://ror.org/03yxnpp24
dc.type.versioninfo:eu-repo/semantics/publishedVersiones
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.contributor.affiliationUniversidad de Sevilla. Departamento de Medicinaes
dc.relation.publisherversionhttps://www.mdpi.com/2072-6694/14/1/192/htmes
dc.identifier.doi10.3390/cancers14010192es
dc.journaltitleCancerses
dc.publication.volumen14es
dc.publication.issue1es

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