Browsing by Author "Tezcanli, Burcin"

Now showing 1 - 2 of 2

Enalapril-induced Apoptosis of Acute Promyelocytic Leukaemia Cells Involves STAT5A
(int inst Anticancer Research, 2012) Purclutepe, Ozlem; Iskender, Guniz; Kiper, Hatice Demet; Tezcanli, Burcin; Selvi, Nur; Avci, Cigir Biray; Saydam, Guray
Background: In this study, we aimed at evaluating the cytotoxic and apopotic effects of enalapril on human HL60 acute promyelocytic leukaemia cells and at clarifying the roles of signal transducers and activator of transcription proteins (STATs) on enalapril-induced cell death. Materials and Methods: Cell viability and cytotoxicity tests were conducted by Trypan blue dye exclusion and 2,3-Bis[2-methoxy-4-nitro-5-sulphophenyl]-2H-tetrazolium-5-carboxanilide inner salt (XTT) assays, respectively. Apoptotic analyses were performed by the Annexin V-enhanced green fluorescent protein (EGFP) staining method and by fluorescence microscopy. Expression levels of STAT3, -5A and -5B genes were analysed by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). Results: The results showed that enalapril reduced viability and proliferation, and induced apoptosis in HL60 cells in a dose- and time-dependent manner as compared to untreated controls. The expression levels of STAT5A gene were significantly reduced in enalapril-treated HL60 cells as compared to untreated controls. Conclusion: Taken together, all data showed for the first time that enalapril has significant anticancer potential for the treatment of acute premyelocytic leukaemia.
Suppression of STAT5A increases chemotherapeutic sensitivity in imatinib-resistant and imatinib-sensitive K562 cells
(Taylor & Francis Ltd, 2010) Kosova, Buket; Tezcanli, Burcin; Ekiz, Huseyin Atakan; Cakir, Zeynep; Selvi, Nur; Dalmizrak, Aysegul; Baran, Yusuf; Baran, Yusuf
STAT proteins are cytoplasmic transcription factors that are involved in the regulation of numerous cellular activities such as cell growth, differentiation, and survival. In this study, we aimed to identify the expression pattern of STAT genes in imatinib-sensitive and -resistant K562 cells, and further, to reveal the effects of STAT5A siRNA knockdown on cell growth and apoptosis induction. The XTT cell proliferation assay showed that both sensitive and resistant K562 cells were sensitized to imatinib upon transfection with STAT5A siRNA. Caspase-3 enzyme activity was increased significantly in both cells. These results may open up new opportunities to overcome chemotherapeutic resistance in leukemia.