Browsing by Author "Ceylan, Onur"

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Assessment of the Neuroprotective Potential of D-Cycloserine and L-Serine in Aluminum Chloride-Induced Experimental Models of Alzheimer's Disease: In Vivo and In Vitro Studies
(Frontiers Media SA, 2022) Tozlu, OEzlem OEzdemir; Tuerkez, Hasan; Okkay, Ufuk; Ceylan, Onur; Bayram, Cemil; Hacimueftueoglu, Ahmet; Mardinoglu, Adil
Alzheimer's disease (AD) is a neurodegenerative disease characterized by the accumulation of amyloid-beta (A beta) plaques and neurofibrillary tangles in the brain accompanied by synaptic dysfunction and neurodegeneration. No effective treatment has been found to slow the progression of the disease. Therapeutic studies using experimental animal models have therefore become very important. Therefore, this study aimed to investigate the possible neuroprotective effect of D-cycloserine and L-serine against aluminum chloride (AlCl3)-induced AD in rats. Administration of AlCl3 for 28 days caused oxidative stress and neurodegeneration compared to the control group. In addition, we found that aluminum decreases alpha -secretase activity while increasing beta -secretase and gamma -secretase activities by molecular genetic analysis. D-cycloserine and L-serine application resulted in an improvement in neurodegeneration and oxidative damage caused by aluminum toxicity. It is believed that the results of this study will contribute to the synthesis of new compounds with improved potential against AlCl3-induced neurodegeneration, cognitive impairment, and drug development research.
CASC11 Promotes Aggressiveness of Prostate Cancer Cells Through miR145/Igf1r Axis
(Springer Nature, 2021) Capik, Ozel; Sanli, Fatma; Kurt, Ali; Ceylan, Onur; Suer, Ilknur; Kaya, Murat; Karatas, Omer Faruk
Background Prostate cancer (PCa) is the most common malignancy diagnosed among men after lung cancer in developed countries. Investigation of the underlying molecular mechanisms of PCa is urgently needed in order to develop better therapeutic strategies and to reveal more effective therapeutic targets. In this study, we aimed at exploring the potential functions of CASC11 in association with miR-145 and IGF1R during the malignant progression of PCa cells. Methods We initially investigated the oncogenic potential of noncoding members of CASC gene family and analyzed the effects of CASC11 overexpression on proliferation, migration, and colony formation ability of DU145, LNCaP, and PC3 PCa cells. We, then, exprlored the association of CASC11, miR-145, and IGF1R expression and their impacts on PI3K/AKT/mTOR signaling pathway in in vitro models. Results In silico analysis revealed that of the CASC family only CASC11 showed consistent results considering its differential expression as well as its association with the overall survival of patients. We demonstrated that ectopic overexpression of CASC11 significantly increased the proliferation, colony formation, and migration capacity in all three cell lines. CASC11 overexpression caused suppression of miR-145 and overexpression of IGF1R, leading to activation of PI3K/AKT/mTOR signaling pathway. Conclusion In summary, we found that CASC11 is upregulated in PCa cells and clinical tumor samples in comparison to corresponding controls and revealed that ectopic CASC11 overexpression promotes cellular phenotypes associated with PCa progression through CASC11/miR-145/IGF1R axis.
In Vitro and In Vivo Neuroprotective Effects of Sarcosine
(Wiley, 2022) Tanas, Arzuguel; Tozlu, Ozlem Ozdemir; Gezmis, Tugba; Hacimueftueoglu, Ahmet; Abd El-Aty, A. M.; Ceylan, Onur; Tuerkez, Hasan
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by behavioral and psychological symptoms in addition to cognitive impairment and loss of memory. The exact pathogenesis and genetic background of AD are unclear and there remains no effective treatment option. Sarcosine, an n-methyl derivative of glycine, showed a promising therapeutic strategy for some cognitive disorders. To our knowledge, the impacts of sarcosine supplementation against AD have not yet been elucidated. Therefore, we aimed to determine the neuroprotective potential of sarcosine in in vitro and in vivo AD model. In vitro studies have demonstrated that sarcosine increased the percentage of viable cells against aluminum induced neurotoxicity. In AlCl3-induced rat model of AD, the level of antioxidant capacity was significantly decreased and expression levels of APP, BACE1, TNF-alpha, APH1A, and PSENEN genes were elevated compared to the control group. Additionally, histopathological examinations of the hippocampus of AlCl3-induced rat brains showed the presence of neurofibrillary tangles (NFTs). However, the administration of sarcosine produced marked improvement and protection of AD-associated pathologies induced by AlCl3 in experimental rats. Therefore, this investigation may contribute to design novel therapeutic strategies using sarcosine for the management of AD pathologies.