Yazar "Celik, Besne" seçeneğine göre listele

Listeleniyor 1 - 2 / 2
  • Küçük Resim Yok
    Öğe
    Nilotinib exerts a therapeutic approach via JAK/STAT pathway and cytokine network in chronic myeloid leukemia cells
    (2024) Yavuz, Tunzale; Kaymaz, Burcin Tezcanli; Celik, Besne; Takanlou, Leila Sabour; Alcitepe, İlayda; Takanlou, Maryam Sabour; Avci, Cigir Biray
    Aim: 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.
  • Küçük Resim Yok
    Öğe
    Ponatinib and STAT5 Inhibitor Pimozide Combined Synergistic Treatment Applications Potentially Overcome Drug Resistance via Regulating the Cytokine Expressional Network in Chronic Myeloid Leukemia Cells
    (Mary Ann Liebert, Inc, 2024) Tezcanli Kaymaz, Burcin; Gumus, Nurcan; Celik, Besne; Alcitepe, Ilayda; Biray Avci, Cigir; Aktan, Cagdas
    Chronic myeloid leukemia (CML) is a clonal myeloproliferative hematological disease characterized by the chimeric breakpoint-cluster region/Abelson kinase1 (BCR