Browsing by Author "Avci, Cigir Biray"

Now showing 1 - 7 of 7

Citation - WoS: 0
Autophagic and Apoptotic Effects of Tyrosine Kinase Inhibitors in Myeloid Leukemia: Comparison of Three Generation
(Amer Soc Hematology, 2012) Kayabasi, Cagla; Avci, Cigir Biray; Susluer, Sunde Yilmaz; Balci, Tugce; Baran, Yusuf; Saydam, Guray; Gunduz, Cumhur; Baran, Yusuf
[No Abstract Available]
Citation - WoS: 22
Caffeic acid phenethyl ester triggers apoptosis through induction of loss of mitochondrial membrane potential in CCRF-CEM cells
(Springer, 2011) Avci, Cigir Biray; Gunduz, Cumhur; Baran, Yusuf; Sahin, Fahri; Yilmaz, Sunde; Dogan, Zeynep Ozlem; Saydam, Guray; Baran, Yusuf
CAPE (caffeic acid phenethyl ester) is one of the most valuable and investigated component of propolis which is composed by honeybees. In the current study, we aimed at examining apoptotic effects of CAPE on CCRF-CEM leukemic cells and at determining the roles of mitochondrial membrane potential (MMP) in cell death. Trypan blue and XTT methods were used to evaluate the cytotoxicity. Apoptosis was examined by ELISA-based oligonucleotide and acridine orange/ethidium bromide dye techniques. Loss of mitochondrial membrane potential was evaluated using JC-1 dye by flow cytometric analysis and under fluorescent microscope. We detected the time- and dose-dependent increases in cytotoxic effect of CAPE on CCRF-CEM cells. ELISA and acridine orange/ethidium bromide results showed that apoptotic cell population increased significantly in CCRF-CEM cells exposed to increasing concentrations of CAPE. On the other hand, there was significant loss of MMP determined in response to CAPE in CCRF-CEM cells. This in vitro data by being supported with clinical data may open the way of the potential use of CAPE for the treatment of leukemia.
Citation - WoS: 10
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.
Citation - WoS: 0
Investigating the potential therapeutic role of targeting STAT3 for overcoming drug resistance by regulating energy metabolism in chronic myeloid leukemia cells
(Mashhad Univ Med Sciences, 2022) Kaymaz, Burcin Tezcanli; Gunel, Nur Selvi; Sogutlu, Fatma; Ay, Neslihan Pinar Ozates; Baran, Yusuf; Gunduz, Cumhur; Avci, Cigir Biray; Baran, Yusuf
Objective(s): STATs are one of the initial targets of emerging anti-cancer agents due to their regulatory roles in survival, apoptosis, drug response, and cellular metabolism in CML. Aberrant STAT3 activity promotes malignancy, and acts as a metabolic switcher in cancer cell metabolism, contributing to resistance to TKI nilotinib. To investigate the possible therapeutic effects of targeting STAT3 to overcome nilotinib resistance by evaluating various cellular responses in both sensitive and nilotinib resistant CML cells and to test the hypothesis that energy metabolism modulation could be a mechanism for re-sensitization to nilotinib in resistant cells. Materials and Methods: By using RNAi-mediated STAT3 gene silencing, cell viability and proliferation assays, apoptotic analysis, expressional regulations of STAT mRNA transcripts, STAT3 total, pTyr705, pSer727 protein expression levels, and metabolic activity as energy metabolism was determined in CML model K562 cells, in vitro. Results: Targeting STAT3 sensitized both parental and especially nilotinib resistant cells by decreasing leukemic cell survival; inducing leukemic cell apoptosis, and decreasing STAT3 mRNA and protein expression levels. Besides, cell energy phenotype was modulated by switching energy metabolism from aerobic glycolysis to mitochondrial respiration in resistant cells. RNAi-mediated STAT3 silencing accelerated the sensitization of leukemia cells to nilotinib treatment, and STAT3-dependent energy metabolism regulation could be another underlying mechanism for regaining nilotinib response. Conclusion: Targeting STAT3 is an efficient strategy for improving the development of novel CML therapeutics for regaining nilotinib response, and re-sensitization of resistant cells could be mediated by induced apoptosis and regulation in energy metabolism.
Citation - WoS: 30
Quercetin-induced apoptosis involves increased hTERT enzyme activity of leukemic cells
(Taylor & Francis Ltd, 2011) Avci, Cigir Biray; Yilmaz, Sunde; Dogan, Zeynep Ozlem; Saydam, Guray; Dodurga, Yavuz; Ekiz, Huseyin Atakan; Gunduz, Cumhur
We aimed to examine the growth suppressive effects of quercetin on acute promyelocytic and lymphoblastic leukemia and chronic myeloid leukemia, and to find out whether the growth suppression is related to the blocking of telomerase enzyme activity. Cytotoxic effects of quercetin were shown by trypan blue analyses. Apoptotic effects of quercetin were examined by acridine orange and ethidium bromide staining by fluorescence microscopy. The effects of quercetin on telomerase enzyme activity were shown by hTERT Quantification Kit. Our results demonstrated that quercetin has antiproliferative and apoptotic effects on T-cell acute lymphoblastic leukemia (ALL), acute promyelocytic leukemia, and chronic myeloid leukemia (CML) cells. We also showed for the first time by this study that quercetin suppresses the activity of telomerase in ALL and CML cells. The results of this study show the importance of quercetin for its therapeutic potential in treatment of leukemias.
Citation - WoS: 12
STAT pathway in the regulation of zoledronic acid-induced apoptosis in chronic myeloid leukemia cells
(Elsevier France-editions Scientifiques Medicales Elsevier, 2013) Kiper, Hatice Demet; Kaymaz, Burcin Tezcanli; Gokbulut, Aysun Adan; Selvi, Nur; Avci, Cigir Biray; Kosova, Buket; Saydam, Guray
In this study, we aimed to evaluate the cytotoxic and apoptotic effects of zoledronic acid on K562 chronic myeloid leukemia (CML) cells and to examine the roles of STAT genes on zoledronic acid-induced apoptosis. The results showed that zoledronic acid decreased proliferation, and induced apoptosis in K562 cells in a dose- and time-dependent manner. mRNA and protein levels of STAT3, -5A and -5B genes were significantly reduced in zoledronic acid-treated K562 cells. These data indicated that STAT inhibition by zoledronic acid may be therapeutic in CML patients following the confirmation with clinical studies. (C) 2013 Elsevier Masson SAS. All rights reserved.
Citation - WoS: 17
Use of MicroRNAs in Personalized Medicine
(Humana Press inc, 2014) Avci, Cigir Biray; Baran, Yusuf; Baran, Yusuf
Personalized medicine comprises the genetic information together with the phenotypic and environmental factors to yield healthcare tailored to an individual and removes the limitations of the "one-size-fits-all" therapy approach. This provides the opportunity to translate therapies from bench to clinic, to diagnose and predict disease, and to improve patient-tailored treatments based on the unique signatures of a patient's disease and further to identify novel treatment schedules. Nowadays, tiny noncoding RNAs, called microRNAs, have captured the spotlight in molecular biology with highlights like their involvement in DNA translational control, their impression on mRNA and protein expression levels, and their ability to reprogram molecular signaling pathways in cancer. Realizing their pivotal roles in drug resistance, they emerged as diagnostic targets orchestrating drug response in individualized therapy examples. It is not premature to think that researchers could have the US Food and Drug Administration (FDA)-approved kit-based assays for miRNA analysis in the near future. We think that miRNAs are ready for prime time.