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    Assessment of structural protein expression by FTIR and biochemical assays as biomarkers of metabolites response in gastric and colon cancer
    (Elsevier B.V., 2021) Güleken, Zozan; Bulut, Huri; Gültekin, Güldal İnal; Arıkan, Soykan; Yaylım, İlhan; Hakan, Mehmet Tolgahan; Sönmez, Dilara; Tarhan, Nevzat K.; Depciuch, Joanna
    Colon and gastric cancers are the widespread benign types of cancers which are synchronous and metachronous neoplasms. In terms of the progression and progress of the disease, metabolic processes and differentiation in protein structures have an important role in for treatment of the disease. In this study we proposed to investigate the metabolic process and the differentiation of protein secondary structure among colon and gastric cancer as well as healthy controls using biochemistry and Fourier Transform InfraRed spectroscopy (FTIR) methods. For this purpose, we measured blood serum of 133 patients, which were conducted upon oncology department (45 colon cancer, 45 gastric cancer and 43 control individuals). The obtained spectroscopic results and biochemical assays showed significant reduction in the amount of functional groups in cancer groups contrary with total protein measurements and structure of protein differences between colon and gastric cancers. Differentiations were visible in serum levels of CEA, CA-125, CA-15-3, CA-19-9 AFP (Alpha fetoprotein) of gastric and colon cancer patients as well as in amide III and secondly described amide I regions. Our findings suggest that amide I bonds in colon cancer cells can be helpful in diagnosis of colon cancer. Indeed, our results showed that metabolic processes were higher in gastric cancer group than in colon cancer. Hence, FTIR spectroscopy and curve-fitting analysis of amide I profile can be successfully applied as tools for identifying quantitative and qualitative changes of proteins in human cancerous blood serum. However, what is very important, in PCA analysis we see, that the scatter plot of PC1 (variability 80%) and PC2 (variability 15%) show that the data related to the control and two cancer groups are clustered together with different magnitudes and directions.
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    Association of the kynurenine pathway metabolites with clinical, cognitive features and IL-1 beta levels in patients with schizophrenia spectrum disorder and their siblings
    (ELSEVIER, 2021) Noyan, Handan; Erdağ, Ece; Tüzün, Erdem; Yaylim, Lhan; Küçükhüseyin, Özlem; Hakan, Mehmet Tolgahan; Gülöksüz, Sinan; Rutten, Bart P. F.; Saka, Meram Can; Atbaşoğlu, Cem; Alptekin, Köksal; Van Os, Jim; Uçok, Alp
    Objective: There is evidence suggesting that tryptophan (TRP)-kynurenine (KYN) pathway dysregulation is involved in the pathophysiology of schizophrenia and is regulated by inflammatory cytokines. The study investigate for the first time whether this dysregulation occurs in advanced stages of the disease as a byproduct or emerges as one of the early and inherited manifestations of schizophrenia. Method: Sera of 148 patients with schizophrenia spectrum disorders (SCZ), 139 unaffected siblings (SIB) and 210 controls were investigated. Serum interleukin (IL)-1 beta levels were measured by ELISA, and TRP, KYN and kynurenic acid (KYNA) levels were measured by a high-performance liquid chromatography system. Also, we collected clinical data by applying Comprehensive Assessment of Symptoms and History in SCZ, and SIS-R in SIB and control groups. Results: Compared to controls, SCZ and SIB groups had lower TRP and higher KYNA levels. TRP levels showed significant differences only between SCZ and controls (p < 0.01). KYNA levels of both SCZ (p <_ 0.001) and SIB (p < 0.05) were higher than controls. No statistical significance was found for KYN levels across groups. SCZ and SIB groups had higher serum IL-1 beta levels than controls (p <_ 0.001). Conclusions: Patients with SCZ and their siblings exhibited similar clinical features and TRP metabolite levels suggesting that TRP-KYN dysregulation may be an inherited component of the disease putatively conferring increased risk to schizophrenia. Elevation of IL-1 beta is one of the factors promoting overconsumption of the TRP-KYN pathway leading to increased production of neuroregulatory KYNA and presumably to neurodegeneration. (c) 2021 Elsevier B.V. All rights reserved.
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    Investigation of possible associations between tryptophan/kynurenine status and FOXP3 expression in colorectal cancer
    (Taylor and Francis, 2022) Ay, Ebru Nur; Hakan, Mehmet Tolgahan; Arıkan, Soykan; Demirkol, Şeyda; Doğan, Mehmet Baki; Hepokur, Ceylan Özsoy; Yaylım, İlhan; Akyüz, Filiz; Horozoğlu, Cem
    Tryptophan metabolism in the tumor microenvironment exerts immunosuppressive effects by affecting the anti-tumor functions of immune cells. The immunosuppressive roles of tryptophan and tryptophan metabolites and their effects on the FOXP3 gene, highly expressed in regulatory T cells (Tregs), are remarkable. Our study aimed to investigate the relation between tryptophan metabolism and the transcription factor FOXP3 gene in colorectal cancer (CRC). Patients with CRC (n?=?159) and controls (n?=?112) were included in the study. The FOXP3 rs3761548 variant genotyping from the isolated genomic DNA was performed by PCR-RFLP. FOXP3 gene expression was determined by Q-PCR in RNAs isolated from resected tissues at the same time. Serum tryptophan, kynurenine, kynurenic acid levels of the cases were determined by HPLC. In serum samples with CRC, tryptophan level was 14.32?±?1.09??mol/L, kynurenine level was 1.33?±?0.02??mol/L, and the kynurenic acid level was 0.01?±?0.001??mol/L. The level of tryptophan was found to be low in CRC compared to control (p?
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    Regulation of Nrf2/Keap1 signaling pathway in cancer drug resistance by galectin-1: cellular and molecular implications
    (Oae Publishing Inc, 2024) Yaylim, Ilhan; Aru, Melek; Farooqi, Ammad Ahmad; Hakan, Mehmet Tolgahan; Buttari, Brigitta; Arese, Marzia; Saso, Luciano
    Oxidative stress is characterized by the deregulation of the redox state in the cells, which plays a role in the initiation of various types of cancers. The activity of galectin-1 (Gal -1) depends on the cell redox state and the redox state of the microenvironment. Gal -1 expression has been related to many different tumor types, as it plays important roles in several processes involved in cancer progression, such as apoptosis, cell migration, adhesion, and immune response. The erythroid-2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap1) signaling pathway is a crucial mechanism involved in both cell survival and cell defense against oxidative stress. In this review, we delve into the cellular and molecular roles played by Gal -1 in the context of oxidative stress onset in cancer cells, particularly focusing on its involvement in activating the Nrf2/Keap1 signaling pathway. The emerging evidence concerning the anti-apoptotic effect of Gal -1, together with its ability to sustain the activation of the Nrf2 pathway in counteracting oxidative stress, supports the role of Gal -1 in the promotion of tumor cells proliferation, immuno-suppression, and anti -tumor drug resistance, thus highlighting that the inhibition of Gal -1 emerges as a potential strategy for the restraint and regression of tumor progression. Overall, a deeper understanding of the multi -functionality and disease -specific expression profiling of Gal -1 will be crucial for the design and development of novel Gal -1 inhibitors as anticancer agents. Excitingly, although it is still understudied, the ever-growing knowledge of the sophisticated interplay between Gal -1 and Nrf2/Keap1 will enable researchers to gain valuable insights into the underlying causes of carcinogenesis and metastasis.