Köse, Sıla Naz

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https://hdl.handle.net/20.500.14365/7080
Name Variants
Köse, S.N.
Köse, Sila Naz
Koese, Sila Naz
Kose, Sila Naz
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sila.kose@ieu.edu.tr
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05.08. Genetics and Bioengineering
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Current Staff
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0000-0003-2358-1605
Scopus Author ID
58189346900
Turkish CoHE Profile ID
E0095F096963FD3B
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WoS Researcher ID
HZH-5954-2023
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Sila_Naz_Kose.jpg (15.73 KB)

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  • Thumbnail Image
    Article
    Expressions of the Satellite Repeat Hsat5 and Transposable Elements Are Implicated in Disease Progression and Survival in Glioma
    (Tubitak Scientific & Technological Research Council Turkey, 2024) Köse, Sıla Naz; Yaraş, Tutku; Bursalı, Ahmet; Oktay, Yavuz; Yandım, Cihangir; Karakulah, Gökhan
    The glioma genome encompasses a complex array of dysregulatory events, presenting a formidable challenge in managing this devastating disease. Despite the widespread distribution of repeat and transposable elements across the human genome, their involvement in glioma's molecular pathology and patient survival remains largely unexplored. In this study, we aimed to characterize the links between the expressions of repeat/transposable elements with disease progression and survival in glioma patients. Hence, we analyzed the expression levels of satellite repeats and transposons along with genes in low-grade glioma (LGG) and high-grade glioma (HGG). Endogenous transposable elements LTR5 and HERV_a-int exhibited higher expression in HGG patients, along with immune response-related genes. Altogether, 16 transposable elements were associated with slower progression of disease in LGG patients. Conversely, 22 transposons and the HSAT5 satellite repeat were linked to a shorter event-free survival in HGG patients. Intriguingly, our weighted gene coexpression network analysis (WGCNA) disclosed that the HSAT5 satellite repeat resided in the same module network with genes implicated in chromosome segregation and nuclear division; potentially hinting at its contribution to disease pathogenesis. Collectively, we report for the first time that repeat and/or transposon expression could be related to disease progression and survival in glioma. The expressions of these elements seem to exert a protective effect during LGG-to-HGG progression, whereas they could have a detrimental impact once HGG is established. The results presented herein could serve as a foundation for further experimental work aimed at elucidating the molecular regulation of glioma genome.
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    Article
    Citation - WoS: 1
    Citation - Scopus: 1
    Thyroid Hormone T3 Augments the Cytotoxicity of Sorafenib in Huh7 Hepatocellular Carcinoma Cells by Suppressing Akt Expression
    (Wolters Kluwer Medknow Publications, 2024) Uyulgan, S.; Köse, S.N.; Kıpçak, A.; Başkan, Y.; Dağlar, G.; Karagonlar, Z.F.; Yandım, C.
    Background and Objectives: Hepatocellular carcinoma (HCC) is a primary cancer that poorly responds to treatment. Molecular cancer studies led to the development of kinase inhibitors, among which sorafenib stands out as a multi-kinase inhibitor approved by FDA for first line use in HCC patients. However, the efficiency of sorafenib was shown to be counteracted by numerous subcellular pathways involving the effector kinase AKT, causing resistance and limiting its survival benefit. On the way of breaking such resistance mechanisms and increase the efficiency of sorafenib, deeper understanding of hepatocellular physiology is essential. Thyroid hormones were shown to be metabolized in liver and inevitably affect the molecular behaviour of hepatocytes. Interestingly, thyroid hormone T3 was also demonstrated to be potentially influential in liver regeneration and treatment with this hormone reportedly led to a decrease in HCC tumor growths. In this study, we aimed to uncover the impact of T3 hormone on the cytotoxic response to sorafenib in HCC in vitro. Materials and Methods: We pre-treated the HCC cell line Huh-7 with T3 prior to sorafenib exposure both in 2D and 3D culture. We checked cell viability with MTT assay in 2D culture and measured the sizes of 3D spheroids with bright-field microscopy followed by a surface analysis with ImageJ. We also performed scratch assay to measure cell migration as well as western blot and qPCR to uncover affected pathways. Results: We observed an additive effect to sorafenib’s cytotoxicity both in 2D and 3D culture. Cell migration assay also confirmed our finding and pointed out a benefit of T3 hormone in HCC cell migration. Western blot experiments showed that T3 exerts its additive effect by suppressing AKT expression upon sorafenib treatment both at protein and gene expression levels. Conclusion: Our results open a promising new avenue in increasing sorafenib’s cytotoxicity where thyroid hormone T3 is utilized to modulate AKT expression to combat resistance, and warrant further studies in the field. © 2024 Journal of Cancer Research and Therapeutics | Published by Wolters Kluwer - Medknow.
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    Article
    Citation - WoS: 11
    Citation - Scopus: 11
    Characterization of Cisplatin Loaded Hydrophilic Glycol Chitosan Modified Eumelanin Nanoparticles for Potential Controlled-Release Application
    (Elsevier, 2023) Atik, Aleyna; Günal, Tuğce; Acar Bozkurt, Pınar; Kose, Sila Naz; Alp, Burcak; Yandım, Cihangir; Kaleli, Nurettin Mete
    Free liquid cytotoxic substances, such as cisplatin (CDDP), have been widely administered for the conventional chemotherapy treatment of cancer patients. However, this classical approach has several drawbacks, including high dosage requirements, poor bioavailability, low therapeutic index, and geno-/cyto-toxicity resulting in several adverse side effects that constrain patient compliance and clinical outcomes. Such downsides can be improved by replacing conventional drugs with advanced nanocomposite-drug conjugates. In line with this, our study aimed to characterize a novel potential drug nano delivery system, so-called hydrophilic glycol chitosan (HGC) coated melanin nanoparticles (MNPs), to improve the abovementioned constraints in the case of classical chemotherapy drug cisplatin. Following the production of MNP-based nanocomplexes by a single-step mixing, essential physical and chemical characterizations were performed. The nanoformulations generated here were spherically shaped with an optimum size range (between 100 and 200 nm) and exhibited comparable drug loading capacities (21.7% +/- 0.5 for the CDDP-MNPs and 24.7% +/- 0.4 for HGC/CDDP-MNPs) and remarkable entrapment efficiencies (93.2% +/- 2.0 for CDDP-MNPs and 94.9% +/- 1.1 for HGC/CDDP-MNPs) as a biopolymer. Notably, the cell viability assay showed that MNP-based nanocarriers could inhibit the proliferation of liver cancer cells in a more prolonged fashion compared to free CDDP. The TGA and FTIR-ATR analyses confirmed the compatibility between CDDP and its nanocarrier MNP. The Super Case II Transport was primarily in charge of controlling CDDP release from both matrices as a result of polymer relaxation and swelling of HGC-CDDP-MNPs and CDDP-MNPs, which is highly preferred because it enables simple manipulation of the nanocarrier properties to suit the disease biology. All of these findings point to the natural MNP-based nanoformulation's superiority as a prospective and cutting-edge chemotherapeutic nano-delivery technology.
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    Master Thesis
    Synoptic Mapping of Dna Damage in the Replicative Senescence of Human Fibroblasts
    (İzmir Ekonomi Üniversitesi, 2023) Köse, Sila Naz; Yandım, Ci̇hangi̇r
    Hücrenin doğal yaşlanmasıyla ilişkilendirilen replikatif senesans, büyüme duraklaması ve immün fenotiple ayırt edilir. Telomer kısalamasıyla DNA hasarı arasındaki güçlü bağlantı, senesansın temelinde tanınmış olsa da, çalışmalar, telomer uzunluğundan bağımsız olarak replikatif senesansın potansiyeline işaret etmektedir. Özellikle, replikatif senesans sırasında telomer dışında DNA hasarının biriktiği bildirilmiştir, ancak bu süreçte etkilenen belirli genomik bölgeler henüz belirsiz kalmaktadır. Bu tez, replikatif senesans sırasında endojen DNA hasarını haritalamayı ve DNA hasarına yatkın insan genomunun bölgelerini tanımayı amaçlamaktadır. Ana araştırma motivasyonu, hücresel yaşlanma sırasında muhtemelen mutasyona uğrayan genleri, düzenleyici elementleri ve tekrarlanan motifleri açığa çıkarmaktır. Fibroblast senesans modelinden yararlanarak, genç, erken yaşlı ve geç yaşlı hücrelerin moleküler karakterizasyonu yapılmıştır. Bu süreci takiben, γ-H2AX DNA hasar belirteci ile kromatin immünopresipitasyonu ve yeni nesil dizileme yapılmıştır. Şaşırtıcı bir şekilde, γ-H2AX mekanizmalarının sadece telomerik bölgelerde değil, aynı zamanda gen zengin bölgelerde, düzenleyici elementlerde ve LINE, SINE ve çeşitli satelit dizileri gibi tekrarlanan DNA'lar içinde de görüldüğü gözlemlenmiştir. Bu, replikatif senesans sırasında meydana gelen endojen DNA hasarının sadece telomerlerle sınırlı olmadığını göstermektedir. Ayrıca, gen ontoloji analizi, etkilenen genlerin bağışıklık sistemi aktivasyonu, hücre ölümü, damarlaşma, diyabet ve kanserle ile ilgili olduğunu ortaya koymuştur. Bulgularımız, mutasyonların yaşlanan genomda rastgele birikmediğini, bunun yerine hücrelerin senesansa ilerlerken bilinen yaşa bağlı fenotiplere ve hastalıklara yönelik belirgin bir eğilim gösterebileceğini düşündürmektedir. Bu yeni bilgi, yaşlanma süreçlerinin anlaşılmasını zenginleştirmekte ve yaşla ilişkili hastalıklarda DNA hasarına yönelik müdahalelerin geliştirilmesine rehberlik edebilir. Bu tez, TÜBİTAK 3501 programından (Proje No: 219Z371) fon desteği almıştır.