Nilotinib exerts a therapeutic approach via JAK/STAT pathway and cytokine network in chronic myeloid leukemia cells

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dc.contributor.authorYavuz, Tunzale
dc.contributor.authorKaymaz, Burcin Tezcanli
dc.contributor.authorCelik, Besne
dc.contributor.authorTakanlou, Leila Sabour
dc.contributor.authorAlcitepe, İlayda
dc.contributor.authorTakanlou, Maryam Sabour
dc.contributor.authorAvci, Cigir Biray
dc.date.accessioned2024-08-31T07:32:05Z
dc.date.available2024-08-31T07:32:05Z
dc.date.issued2024
dc.departmentEge Üniversitesien_US
dc.description.abstractAim: Chronic myeloid leukemia (CML) displays a constitutive tyrosine kinase (TK) activity which in turn leads to the activation of various signaling pathways and the outcome of leukemic phenotype. Activated STAT5A and STAT5B from JAK/STAT pathway induce cell growth, proliferation, differentiation, and survival of leukemic cells which are promoted by a cytokine network. Since the second-generation tyrosine kinase inhibitor nilotinib has the advantage of inhibiting this oncogenic TK activity; we aimed to investigate the underlying mechanism of its therapeutic approach and how it induced apoptosis via analyzing the forthcoming molecular targets of the pathway. Materials and Methods: By Nilotinib treatments, cell viability and proliferation assays, apoptotic analysis, expressional regulations of STAT5A&5B mRNA transcripts, protein expression levels, and also cytokines’ expressional assessments were determined in CML model K562 cells, in vitro. Results: Nilotinib treatment in a time and dose-dependent manner assessed a therapeutic approach by decreasing leukemic cell proliferation and survival; inducing leukemic cell apoptosis, down regulating STAT5A&5B mRNA, and protein expression levels, and regulating cytokine expressional network. Conclusion: Nilotinib-mediated therapeutics could be dependent on targeting JAK/STAT pathway members STAT5A and STAT5B, besides; regulating the cytokine network might be another underlying mechanism for sensitization and response of K562 cells to nilotinib in leukemia pathogenesis.en_US
dc.identifier.endpage135en_US
dc.identifier.issn1016-9113
dc.identifier.issn2147-6500
dc.identifier.issue1en_US
dc.identifier.startpage124en_US
dc.identifier.trdizinid1227908en_US
dc.identifier.urihttps://search.trdizin.gov.tr/tr/yayin/detay/1227908
dc.identifier.urihttps://hdl.handle.net/11454/103724
dc.identifier.volume63en_US
dc.indekslendigikaynakTR-Dizinen_US
dc.language.isoenen_US
dc.relation.ispartofEge Tıp Dergisien_US
dc.relation.publicationcategoryMakale - Ulusal Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.snmz20240831_Uen_US
dc.subjectNilotiniben_US
dc.subjectchronic myeloid leukemiaen_US
dc.subjectJAK/STAT pathwayen_US
dc.subjectcytokinesen_US
dc.subjectapoptosis.en_US
dc.titleNilotinib exerts a therapeutic approach via JAK/STAT pathway and cytokine network in chronic myeloid leukemia cellsen_US
dc.typeArticleen_US

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