Induction of apoptosis and autophagy via regulation of AKT and JNK mitogen-activated protein kinase pathways in breast cancer cell lines exposed to gold nanoparticles loaded with TNF-? and combined with doxorubicin

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dc.contributor.authorJawad, Marwa H.
dc.contributor.authorJabir, Majid S.
dc.contributor.authorÖztürk, Kamile
dc.contributor.authorSulaiman, Ghassan M.
dc.contributor.authorAbomughaid, Mosleh M.
dc.contributor.authorAlbukhaty, Salim
dc.contributor.authorAl-Kuraishy, Hayder M.
dc.contributor.authorAl-Gareeb, Ali I.
dc.contributor.authorAl-Azzawi, Waleed K.
dc.contributor.authorNajm, Mazin A. A.
dc.contributor.authorJawad, Sabrean F.
dc.date.accessioned2024-04-24T06:19:43Z
dc.date.available2024-04-24T06:19:43Z
dc.date.issued2023
dc.departmentSabire Yazıcı Fen Edebiyat Fakültesi
dc.description.abstractGold nanoparticles (GNPs) tagged with peptides are pioneers in bioengineered cancer therapy. The aim of the current work was to elucidate the potential anticancer interactions between doxorubicin and GNPs loaded with tumor necrosis factor-alpha (TNF-?). To investigate whether GNPs loaded with TNF and doxorubicin could stimulate autophagy and apoptosis in breast cancer cells. Two human breast cancer cell lines, MCF-7 and AMJ-13, as well as different apoptotic and autophagy markers, were used. In both cell types, treatment with TNF-loaded GNPs in conjunction with doxorubicin increased the production of apoptotic proteins including Bad, caspase-3, caspase-7, and p53 with upregulation of the LC3-II and Beclin1 proteins. In addition, the findings showed that the mitogen-activated protein kinase signaling pathway was dramatically affected by the GNPs loaded with TNF-? and combined with doxorubicin. This had the effect of decreasing p-AKT while simultaneously increasing p-JNK1/2. The findings demonstrated that GNPs loaded with TNF-? and combined with doxorubicin can induce both autophagy and apoptosis in breast cancer cells. These results suggest that TNF- and doxorubicin-loaded GNPs provide a therapeutic option as a nanomedicine to inhibit the proliferation of breast cancer.
dc.identifier.doi10.1515/ntrev-2023-0148
dc.identifier.issn2191-9089
dc.identifier.issue1en_US
dc.identifier.scopusqualityQ1
dc.identifier.urihttps:/dx.doi.org10.1515/ntrev-2023-0148
dc.identifier.urihttps://hdl.handle.net/20.500.12451/11676
dc.identifier.volume12en_US
dc.identifier.wosWOS:001096076900001
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.language.isoen
dc.publisherWalter de Gruyter GmbH
dc.relation.ispartofNanotechnology Reviews
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectApoptosis
dc.subjectAutophagy
dc.subjectBreast Cell Line
dc.subjectCytotoxicity
dc.subjectDoxorubicin
dc.subjectGNPs
dc.subjectTNF-?
dc.titleInduction of apoptosis and autophagy via regulation of AKT and JNK mitogen-activated protein kinase pathways in breast cancer cell lines exposed to gold nanoparticles loaded with TNF-? and combined with doxorubicin
dc.typeArticle

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