Please use this identifier to cite or link to this item: https://hdl.handle.net/11147/7038
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dc.contributor.authorMacek Jilkova, Zuzana-
dc.contributor.authorZeybek Kuyucu, Ayça-
dc.contributor.authorKurma, Keerthi-
dc.contributor.authorTayébéh, Séyédéh-
dc.contributor.authorPour, Ahmad-
dc.contributor.authorRoth, Gaël S.-
dc.contributor.authorAbbadessa, Giovanni-
dc.contributor.authorYu, Yi-
dc.contributor.authorSchwartz, Brian-
dc.contributor.authorSturm, Nathalie-
dc.contributor.authorMarche, Patrice N.-
dc.contributor.authorHainaut, Pierre-
dc.contributor.authorDecaens, Thomas-
dc.date.accessioned2018-12-12T11:29:52Z-
dc.date.available2018-12-12T11:29:52Z-
dc.date.issued2018-
dc.identifier.citationMacek Jilkova, Z., Zeybek Kuyucu, A., Kurma, K., Tayébéh, S., Pour, A., Roth, G. S.,...Decaens, T. (2018). Combination of AKT inhibitor ARQ 092 and sorafenib potentiates inhibition of tumor progression in cirrhotic rat model of hepatocellular carcinoma. Oncotarget, 8(13), 11145-11158. doi:10.18632/oncotarget.24298en_US
dc.identifier.issn1949-2553-
dc.identifier.issn1949-2553-
dc.identifier.urihttps://doi.org/10.18632/oncotarget.24298-
dc.identifier.urihttp://hdl.handle.net/11147/7038-
dc.description.abstractThe prognosis of patients with advanced hepatocellular carcinoma (HCC) is very poor. The AKT pathway is activated in almost half of HCC cases and in addition, long term exposure to conventional drug treatment of HCC, sorafenib, often results in overactivation of AKT, leading to HCC resistance. Therefore, it is important to assess the safety and the efficacy of selective allosteric AKT inhibitor ARQ 092 (Miransertib) in combination with sorafenib. Here, we demonstrated in vitro that the combination of ARQ 092 with sorafenib synergistically suppressed proliferation, promoted apoptosis, and reduced migration. To test the effect of the combination in vivo, rats with diethylnitrosamine-induced cirrhosis and fully developed HCC were randomized and treated with vehicle, sorafenib, ARQ 092 or the combination of ARQ 092 with sorafenib; (n=7/group) for 6 weeks. Tumor progression, size of tumors and the mean tumor number were significantly reduced by the combination treatment compared to the control or single treatments. This effect was associated with a significant increase in apoptotic response and reduction in proliferation and angiogenesis. Sirius red staining showed a decrease in liver fibrosis. Moreover, treatments improved immune response in blood and in tumor microenvironment. Thus, the combination of ARQ 092 with sorafenib potentiates inhibition of tumor progression and gives the possibility of therapeutic improvement for patients with advanced HCC.en_US
dc.description.sponsorshipLigue contre le Cancer CD63 (2016-R16145CC), The Scientific and Technological Research Council of Turkey (TUBITAK 2214B)en_US
dc.language.isoenen_US
dc.publisherImpact Journalsen_US
dc.relation.ispartofOncotargeten_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.rightsAttribution 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/*
dc.subjectAKT inhibitoren_US
dc.subjectCombination treatmenten_US
dc.subjectDEN-induced modelen_US
dc.subjectFibrosisen_US
dc.subjectLiver cancersen_US
dc.titleCombination of AKT inhibitor ARQ 092 and sorafenib potentiates inhibition of tumor progression in cirrhotic rat model of hepatocellular carcinomaen_US
dc.typeArticleen_US
dc.institutionauthorZeybek Kuyucu, Ayça-
dc.departmentİzmir Institute of Technology. Bioengineeringen_US
dc.identifier.volume9en_US
dc.identifier.issue13en_US
dc.identifier.startpage11145en_US
dc.identifier.endpage11158en_US
dc.identifier.scopus2-s2.0-85042147926en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.identifier.doi10.18632/oncotarget.24298-
dc.relation.doi10.18632/oncotarget.24298en_US
dc.coverage.doi10.18632/oncotarget.24298en_US
local.message.claim2022-06-09T09:56:55.140+0300|||rp03017|||submit_approve|||dc_contributor_author|||None*
dc.identifier.scopusqualityQ1-
item.openairetypeArticle-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextWith Fulltext-
item.languageiso639-1en-
item.cerifentitytypePublications-
item.grantfulltextopen-
crisitem.author.dept03.01. Department of Bioengineering-
Appears in Collections:Bioengineering / Biyomühendislik
PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
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