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Yavuz, Büşra
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01. Izmir Institute of Technology
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Sustainable Development Goals
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2ZERO HUNGER
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3GOOD HEALTH AND WELL-BEING
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4QUALITY EDUCATION
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5GENDER EQUALITY
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9INDUSTRY, INNOVATION AND INFRASTRUCTURE
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3
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8
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8
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2.67
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2.67
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2
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1
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Article Citation - WoS: 8Citation - Scopus: 8The Role of Connexins in Breast Cancer: From Misregulated Cell Communication To Aberrant Intracellular Signaling(Taylor & Francis, 2022) Yavuz, Büşra; Ünal, Yağmur Ceren; Özçivici, Engin; Meşe Özçivici, Gülistan; 03.01. Department of Bioengineering; 01. Izmir Institute of Technology; 04.03. Department of Molecular Biology and Genetics; 03. Faculty of Engineering; 04. Faculty of ScienceIn spite of clinical advancements and improved diagnostic techniques, breast cancers are the leading cause of cancer-associated deaths in women worldwide. Although 70% of early breast cancers can be cured, there are no efficient therapies against metastatic breast cancers. Several factors including connexins and gap junctions play roles in breast tumorigenesis. Connexins are critical for cellular processes as a linkage between connexin mutations and hereditary disorders demonstrated their importance for tissue homeostasis. Further, alterations in their expression, localization and channel activities were observed in many cancers including breast cancer. Both channel-dependent and independent functions of connexins were reported in initiation and progression of cancers. Unlike initial reports suggesting tumor suppressor functions, connexins and gap junctions have stage, context and isoform dependent effects in breast cancers similar to other cancers. In this review, we tried to describe the current understanding of connexins in tumorigenesis specifically in breast cancers.Publication Connexin26 Mutasyonlarının Neden Olduğu Kid Sendromunda Gözlenen Epidermal Fenotiplerin Oluşmasında Nf-kb Yolağının Rolünün Araştırılması(2024) Yavuz, Büşra; Ünal, Yağmur Ceren; Yıldırım, Meryem Azra; İnal, Ece; Ünal, Yağmur Ceren; Elgin, Resul Gökberk; Öz, Sercan; 01. Izmir Institute of TechnologyConnexinlerin oluşturduğu gap junctionlar ve yarım kanallar insan vücudunda deri gibi bir çok doku ve organın normal olarak faaliyetlerini devam ettirmesinde önemli görevler üstlenirler. Connexin26 (Cx26) mutasyonları hem sendromik olmayan sağırlığa hem de keratitis-ichthyosis-deafness (KID) sendromu gibi deri hastalıklarıyla bağlantılı sendromik sağırlığa neden olmaktadır. Sendromik sağırlığa neden olan mutasyonlar Cx26?nın yeni fonksiyonlar kazanmasına neden olmakta, ancak bunun epidermal hücrelerin fizyolojisini nasıl etkilediği tam olarak bilinmemektedir. Bu projede, KID sendromuna neden olan Cx26-G45E ve Cx26-D50Y mutasyonları ile Cx26-WT içeren HaCaT keratinosit hücrelerinde mutasyonların NF-?B sinyal yolağı moleküllerinin ifadelerine ve NF-?B yolak aktivitesindeki değişimlere etkileri araştırılmıştır. Ayrıca, hücre içi ve hücre dışı kalsiyum konsantrasyonlarının azaltılmasının bu mekanizmalara etkileri sırasıyla BAPTA-AM ve BAPTA kalsiyum çekici molekülleri uygulaması sonucunda incelenmiştir. Son olarak, hücrelerde NF-?B yolağının inhibisyonunun hücrelerin canlılık/çoğalmaları, hücre döngüsü, hücre ölümü ve hücrelerin farklılaşmalarına etkileri tespit edilmiştir. Bu çalışmalar sonucunda, Cx26-D50Y içeren hücrelerde RelB ve c-Rel mRNA ifadesi azalmış, buna karşılık NF-?B yolak aktivitesi artmıştır. Buna karşılık, Cx26-G45E mutasyonunda yolak moleküllerinin ifadelerinde farklılık gözlenmezken yolak aktivitesi azalmıştır. Ayrıca, p65?in Cx26-G45E hücrelerinde Cx26-WT ve Cx26-D50Y?ye kıyasla hem sitoplazmada hem de çekirdekte bulunduğu ve c-Rel proteinin her iki mutasyonda çekirdekte lokalize olduğu tespit edilmiştir. Hücre içi kalsiyumun azalmasının Cx26 overekspresyonu olan hücrelerde RelB?nin çekirdeğe geçişini artırdığı gözlenmiştir. Ayrıyeten, hücre dışı kalsiyumun Cx26-D50Y hücrelerinde p65 ve c-Rel mRNA ifadesini azalttığı tespit edilmiştir. NF-?B inhibisyonu MTT çalışmalarında hücre canlılığını/çoğalmasını azaltmış, ancak, hücre proliferasyonu, döngüsü ve apoptozunu etkilememiştir. Buna karşılık, Cx26-G45E içeren hücrelerde farklılaşma belirteci cytokeratin 10 ve involucrinin arttığı ve cytokeratin 10?daki artışın NF-?B sinyal yolağının inhibisyonu ile azaldığı gözlenmiştir. Sonuç olarak, Cx26 KID sendromu mutasyonlarının NF-?B sinyal yolağına farklı şekillerde etkilerinin olduğu ve bunun hastalarda mutasyona özgü gözlenen epidermal fenotiplerin gelişmesinde rol oynayabileceği değerlendirilmiştir.Master Thesis Investigating the Function of Cx26-I30n and D50y Mutations in Squamous Cell Carcinoma Cell Line Scc-25(01. Izmir Institute of Technology, 2021) Yavuz, Büşra; Meşe Özçivici, Gülistan; Meşe Özçivici, Gülistan; 01. Izmir Institute of Technology; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of ScienceGap junctions are responsible for cell homeostasis and provide cell-cell and cell-ECM communications in multicellular organisms. Gap junction hemichannels consist of connexin (Cx) proteins which functions are crucial for human physiology. Moreover, Cx mutations are associated with various genetic diseases. For example, more than 10 missense mutations in the Cx26 gene cause keratitis-ichthyosis-deafness (KID) syndrome. Among these, Cx26-I30N and Cx26-D50Y cause to form abnormal hemichannels and allow excessive calcium influx into the cell. Furthermore, KID patients have higher squamous cell carcinoma (SCC) incidence and SCC is seen at an earlier age in these patients. Immunohistochemistry stainings have demonstrated aberrant E-cadherin and B-catenin spread in KID patients' samples. In this study, we aimed to effects of Cx26-I30N and Cx26-D50Y mutations associated with KID syndrome in human epithelial SCC cell line SCC-25. For this purpose, stable MSCV, Cx26-WT, Cx26-I30N and Cx26-D50Y cell lines were generated and RTqPCR, Western blotting, immunostaining and MTT assays were done for expression level, localization and viability analysis. For these 4 different cell conditions, a significant increase was detected at Cx26 mRNA levels, but not at protein levels. No difference was found in Cx43 level, which is abundant in epithelial tissue, and was localized in the perinuclear area like Cx26. Additionally, E-cadherin protein levels increased and their localization changed in parallel with the mutations from the perinuclear area to the plasma membrane. Moreover, significant decreases in viability were observed in cells grown in high extracellular Ca2+ medium compared to control in contrast to cells grown in Ca2+-free medium.