Browsing by Author "Oğuz F."

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    Induction of autophagic cell death by thymoquinone in docetaxel resistant prostate cancer cells; [Dosetaksel dirençli prostat kanseri hücrelerinde timokinon tarafından otofajik hücre ölümünün indüklenmesi]
    (Duzce University Medical School, 2021) İlhan S.; Oğuz F.
    Aim: Acquired docetaxel (DOC) resistance of prostate cancer (PCa) is still a clinical problem. In addition to failure in chemotherapy treatment, it causes tumor recurrence. Therefore, novel and more effective compounds are needed in DOC-resistant PCa treatment. This study aimed to investigate the possible cytotoxic and cell death-inducing activities of thymoquinone (TQ), one of the main active components of Nigella sativa L., on DOC-resistant prostate cancer cells. Material and Methods: DOC-resistant PC3 cells (DOC-R/PC3) were developed by the continuous culture with increment concentrations of DOC (1-10 nM) until they improved their growth and division abilities. The cell viability was determined by MTT assay. The Muse™ Annexin V & Dead Cell kit was performed to detect apoptotic cell death. Autophagic vacuoles were observed by staining autophagic vacuoles. The levels of LC3I, LC3II and Beclin-1 proteins were investigated via western blot analysis. Results: TQ inhibited the viability of DOC-R/PC3 cells in a dose-and time-dependent manner (p=0.014). The IC50 value of TQ for DOC-R/PC3 cells was calculated as 60 µM at 72 h. Treatment of TQ did not induce apoptotic cell death in DOC-resistant prostate cancer cells but induced the formation of autophagic vacuoles. Moreover, Beclin-1 and LC3-II protein levels were increased in TQ-treated DOC-R/PC3 cells, however, LC3-I levels were decreased in DOC-R/PC3 cells. Conclusion: All these results show that TQ may become a new therapeutic target for DOC-resistant prostate cancer in the future. © 2021, Duzce University Medical School. All rights reserved.
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    Trabectedin (ET-743) in prostate cancer: Endoplasmic reticulum stress-induced apoptotic effect
    (John Wiley and Sons Inc, 2022) Atmaca H.; Oğuz F.; Ilhan S.
    Trabectedin is a chemotherapy agent originating from a tunicate, Ecteinascidia turbinata. In this study, DNA-independent action mechanisms of trabectedin are investigated in prostate cancer (PCa) cells. Cell viability was assessed via XTT assay. Apoptosis was evaluated via flow cytometry. Tetramethylrodamine ethyl ester (TMRE) dye was utilized to determine mitochondrial membrane potential (MMP). Cell cycle distribution was investigated via flow cytometric analysis. Reactive oxygen species (ROS) were monitored using fluorescence CM-H2DCFDA dye. Changes in CHOP, p-eIF2α, GRP78 and p-PERK which are endoplasmic reticulum (ER) stress-involved proteins were investigated via western blot. Trabectedin induced cytotoxicity and cell cycle arrest at the G2/M phase. Trabectedin decreased MMP via ROS generation in PCa cells. ER stress-related proteins CHOP, p-eIF2α, GRP78 and p-PERK were also elevated by trabectedin treatment indicating the induction of ER stress-induced apoptosis. The results of this study show that trabectedin may be an effective chemotherapeutic for PCa. © 2022 Wiley-VCH GmbH.