Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik

Permanent URI for this collectionhttps://hdl.handle.net/11147/9

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Author: search.filters.author.Pişkin, Özden

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Now showing 1 - 6 of 6
  • Conference Object
    Determination of Cytotoxic and Apoptotic Effects of Caffeic Acid Phenethyl Ester and Gossypol in Combination With Fludarabine at a Molecular Level in Acute Lymphoblastic Leukemia Cells
    (Ferrata Storti Foundation, 2013) Baran, Yusuf; İskender, G.; Pişkin, Özden; Özcan, Mehmet Ali
    [No abstract available]
  • Conference Object
    Diagnostic and Therapeutic Potentials of Expression Levels of Bioactive Sphingolipid Genes in Newly Diagnosed and Drug-Resistant Chronic Myeloid Leukemia Patients
    (Ferrata Storti Foundation, 2013) Baran, Yusuf; Yandım, Melis; Kozanoğlu, İlknur; Özdoğu, Hakan; Pişkin, Özden; Özcan, Mehmet Ali
    [No abstract available]
  • Conference Object
    Antiproliferative and Apoptotic Effects of Resveratrol on Chronic Lymphocytic Leukemia Cells
    (Ferrata Storti Foundation, 2012) Baran, Yusuf; Gökbulut, Aysun; Özcan, Mehmet Ali; Pişkin, Özden; Ünlü, Miray
    [No abstract available]
  • Conference Object
    Expression Levels of Jak/Stat Signaling Genes in Newly Diagnosed, Drug Sensitive and Resistant Chronic Myeloid Leukemia Patients
    (Ferrata Storti Foundation, 2015) Kiraz, Yağmur; Saydam, Güray; Şahin, Fahri; Kozanoğlu, İlknur; Özdoğu, Hakan; Pişkin, Özden; Baran, Yusuf
    [No abstract available]
  • Article
    Citation - WoS: 6
    Citation - Scopus: 7
    Nilotinib Does Not Alter the Secretory Functions of Carotid Artery Endothelial Cells in a Prothrombotic or Antithrombotic Fashion
    (SAGE Publications Inc., 2015) Katgı, Abdullah; Sevindik, Ömer Gökmen; Adan Gökbulut, Aysun; Özsan, Güner Hayri; Yüksel, Faize; Solmaz, Şerife Medeni; Alacacıoğlu, İnci; Özcan, Mehmet Ali; Demirkan, Fatih; Baran, Yusuf; Pişkin, Özden
    Background: There have been concerns about the possible prothrombotic effects of nilotinib, especially in patients having cardiovascular risk factors. The potential mechanism behind the increased risk of thromboembolic events is still not clear. Objectives: In this study, we aimed to evaluate possible harmful effects of nilotinib on endothelial cells. To this aim, we examined proliferative capacity and secretory functions of healthy human carotid artery endothelial cells (HCtAECs) in response to nilotinib. Methods: 3-(4,5-Dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) cell proliferation method was used to determine antiproliferative effects of nilotinib on HCtAECs. The HCtAECs were incubated with 5, 10, and 100 nmol/L doses of nilotinib for 72 hours. Then, in order to assess the endothelial function, levels of nitric oxide (NO), von Willebrand factor (vWF), tissue plasminogen activator, plasminogen activator inhibitor 1 (PAI-1), and endothelin 1 (ET-1) were evaluated using enzyme-linked immunosorbent assay from tissue culture supernatants. Results: There were slight but statistically significant decreases in cell proliferation in response to nilotinib. Nilotinib increased the secretion of t-PA, PAI-1, and vWF in a dose-dependent manner when compared with the untreated control group. The ET-1 secretion was lower in 5 nmol/L and higher in 10 and 100 nmol/L nilotinib-treated cells as compared to untreated cells. Regarding NO secretion, lower levels were observed in 5 and 10 nmol/L, and higher levels were detected in 100 nmol/L nilotinib-treated cells as compared to untreated control group cells. Conclusion: Considering the results obtained in our study, nilotinib does not affect the functions of endothelial cells either in a prothrombotic or an antithrombotic fashion, despite a dose-dependent decline in cell viability.
  • Article
    Citation - WoS: 5
    Citation - Scopus: 7
    The Roles of Antiapoptotic Sphingosine Kinase-1 and Glucosylceramide Genes in Drug Induced Cell Death of Mcf-7 Breast Cancer Cells
    (Zerbinis Medical Publications, 2011) Güçlüler, Gözde; Pişkin, Özden; Baran, Yusuf
    Purpose: Sphingolipids are important signaling molecules mediating cell survival, proliferation, cell cycle regulation and apoptosis. Ceramide is the most vital sphingolipid which induces growth arrest, senescence, and apoptosis. In this study, we aimed to determine the roles of sphingosine kinase- 1 (SK-1) and glucosylceramide synthase (GCS) genes in paclitaxel, doxorubicin, tamoxifen, cyclophosphamide and docetaxel induced apoptosis in human MCF-7 breast cancer cells. Methods: IC50 values (drug concentration inhibiting cell growth by 50%) of the anticancer agents were calculated using XTT cell proliferation assay. Changes in mitochondrial membrane potential (MMP) were determined using JC-1 assay kit. Changes in the mRNA levels of SK-1 and GCS genes were measured by using RT-PCR technique. Results: The results demonstrated significant decrease in cellular proliferation and increase in loss of MMP in a dose-dependent manner. Paclitaxel, doxorubicin, tamoxifen, cyclophosphamide and docetaxel application downregulated SK-1 expression while paclitaxel, tamoxifen, cyclophosphamide and docetaxel but not doxorubicin downregulated GCS comparing to untreated control cells. Conclusion: These results show for the first time that these agents induce apoptosis in MCF-7 cells by downregulating the antiapoptotic SK-1 and GCS genes that may result in accumulation of apoptotic ceramides. © 2011 Zerbinis Medical Publications.