Person: OY, CEREN
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OY
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CEREN
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Publication Investigation of the anticancer mechanism of monensin via apoptosis-related factors in sh-sy5y neuroblastoma cells(Wiley, 2023-08-03) Serter Kocoğlu, Sema; Seçme, Mücahit; Sunay, F. Bahar; Oy, Ceren; OY, CEREN; Tıp Fakültesi; Histoloji ve Embriyoloji Ana Bilim Dalı; AAH-4278-2021Monensin is an ionophore antibiotic that inhibits the growth of cancer cells. The aim of this study was to investigate the apoptosis-mediated anticarcinogenic effects of monensin in SH-SY5Y neuroblastoma cells. The effects of monensin on cell viability, invasion, migration, and colony formation were determined by XTT, matrigel-chamber, wound healing, and colony formation tests, respectively. The effects of monensin on apoptosis were determined by real-time polymerase chain reaction, TUNEL, Western blot, and Annexin V assay. We have shown that monensin suppresses neuroblastoma cell viability, invasion, migration, and colony formation. Moreover, we reported that monensin inhibits cell viability by triggering apoptosis of neuroblastoma cells. Monensin caused apoptosis by increasing caspase-3, 7, 8, and 9 expressions and decreasing Bax and Bcl-2 expressions in neuroblastoma cells. In Annexin V results, the rates of apoptotic cells were found to be 9.66 +/- 0.01% (p < 0.001), 29.28 +/- 0.88% (p < 0.01), and 62.55 +/- 2.36% (p < 0.01) in the 8, 16, and 32 mu M monensin groups, respectively. In TUNEL results, these values were, respectively; 35 +/- 2% (p < 0.001), 34 +/- 0.57% (p < 0.001), and 75 +/- 2.51% (p < 0.001). Our results suggest that monensin may be a safe and effective therapeutic candidate for treating pediatric neuroblastoma.Study HighlightsWHAT IS THE CURRENT KNOWLEDGE ON THE TOPIC?Neuroblastoma is the most common extracranial childhood tumor originating from neural crest cells. Neuroblastomas constitute similar to 15% of childhood cancer deaths. There is a need to develop new and alternative advanced treatment approaches for neuroblastoma oncogenesis. Monensin is an ionophore antibiotic with antiparasitic and antibacterial effects.WHAT QUESTION DID THIS STUDY ADDRESS?No study has been found on the anticancer properties of monensin on neuroblastoma cell proliferation, migration, invasion, and apoptosis. This study addresses dose-dependent and apoptotic pathway-mediated anticarcinogenic properties of monensin in neuroblastoma cells in vitro.WHAT DOES THIS STUDY ADD TO OUR KNOWLEDGE?Monensin suppresses neuroblastoma cell proliferation, invasion, migration, and colony formation. Monensin triggers apoptosis by increasing caspase-3, 7, 8, 9, and cleaved-PARP1 expressions and decreasing Bax and Bcl-2 expressions.HOW MIGHT THIS CHANGE CLINICAL PHARMACOLOGY OR TRANSLATIONAL SCIENCE?Monensin may be a safe and effective therapeutic drug candidate in the treatment of pediatric neuroblastoma.Publication Monensin, an antibiotic isolated from streptomyces cinnamonensis, regulates human neuroblastoma cell proliferation via the PI3K/AKT signaling pathway and acts synergistically with rapamycin(Mdpi, 2023-03-01) Kocoğlu, Sema Serter; Secme, Muecahit; Oy, Ceren; Korkusuz, Gözde; Elmas, Levent; OY, CEREN; Tıp Fakültesi; Histoloji ve Embriyoloji Ana Bilim Dalı; AAH-4278-2021Neuroblastoma is the most common extracranial childhood tumor and accounts for approximately 15% of pediatric cancer-related deaths. Further studies are needed to identify potential therapeutic targets for neuroblastoma. Monensin is an ionophore antibiotic obtained from Streptomyces cinnamonensis with known antibacterial and antiparasitic effects. No study has reported the effects of monensin on SH-SY5Y neuroblastoma cells by targeting the PI3K/AKT signaling pathway. The aim of this study was to investigate the antiproliferative effects of monensin alone and in combination with rapamycin in human SH-SY5Y neuroblastoma cells mediated by the PI3K/AKT signaling pathway. The effects of single and combination applications of monensin and rapamycin on SH-SY5Y cell proliferation were investigated by XTT, and their effects on the PI3K/AKT signaling pathway by RT-PCR, immunohistochemistry, immunofluorescence, and Western blotting. The combined effects of monensin and rapamycin on SH-SY5Y proliferation were most potent at 72 h (combination index < 1). The combination of monensin and rapamycin caused a significant decrease in the expression of P21RAS, AKT, and MAPK1 genes. Single and combined administrations of monensin and rapamycin caused a significant decrease in PI3K/AKT expression. Our results showed for the first time that monensin exerts an antiproliferative effect by targeting the PI3K/AKT signaling pathway in neuroblastoma cells. It is suggested that monensin and its combination with rapamycin may be an effective therapeutic candidate for treating neuroblastoma.Publication Glutamate receptor antagonist suppresses the activation of nesfatin-1 neurons following refeeding or glucose administration(Via Medica, 2022-01-01) Koçoğlu, S. Serter; Oy, C.; Halk, Z.; Çakır, C.; Minbay, Z.; Eyigör, O.; OY, CEREN; Halk, Z.; ÇAKIR, CİHAN; MİNBAY, FATMA ZEHRA; EYİGÖR, ÖZHAN; Tıp Fakültesi; Histoloji ve Embriyoloji Ana Bilim Dalı; 0000-0002-8332-7353; 0000-0003-3463-7483; ABQ-8779-2022; ABE-5128-2020; AAH-5249-2021; ABC-1475-2020Background: Nesfatin-1 is a newly identified satiety peptide that has regulatory effects on food intake and glucose metabolism, and is located in the hypothalamic nuclei, including the supraoptic nucleus (SON). In this study, we have investigated the hypothesis that nesfatin-1 neurons are activated by refeeding and intraperito-neal glucose injection and that the glutamatergic system has regulatory influences on nesfatin-1 neurons in the SON. Materials and methods: The first set of experiments analysed activation of nesfatin-1 neurons after refeeding as a physiological stimulus and the effective-ness of the glutamatergic system on this physiological stimulation. The subjects were randomly divided into three groups: fasting group, refeeding group and antagonist (CNQX + refeeding) group. The second set of experiments analysed activation of nesfatin-1 neurons by glucose injection as a metabolic stimulus and the effectiveness of the glutamatergic system on this metabolic stimulation. The subjects were randomly divided into three groups: saline group, glucose group and antagonist (CNQX + glucose) group. Results: Refeeding significantly increased the number of activated nesfatin-1 neurons by approximately 66%, and intraperitoneal glucose injection activated these neurons by about 55%, compared to the fasting and saline controls. The injections of glutamate antagonist (CNQX) greatly decreased the number of ac-tivated nesfatin-1 neurons. Conclusions: This study suggested that nesfatin-1 neurons were activated by peripheral and/or metabolic signals and that this effect was mediated through the glutamatergic system. (Folia Morphol 2022; 81, 2: 379-386)