Master Degree / Yüksek Lisans Tezleri

Permanent URI for this collectionhttps://hdl.handle.net/11147/3008

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Author: search.filters.author.Yalçın Özuysal, ÖzdenSubject: search.filters.subject.Cancer cells

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  • Master Thesis
    Investigating Oncogenic Role of Sema6d in Breast Cancer Cells
    (Izmir Institute of Technology, 2019) Günyüz, Zehra Elif; Yalçın Özuysal, Özden; Yalçın Özuysal, Özden; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of Technology
    Breast cancer, the most commonly diagnosed cancer type and the leading cause of cancer-associated deaths, is the major health issue among women worldwide. In many cancer types, the expression of the semaphorins and their receptors such as plexins and neuropilins are dysregulated. SEMA6D is a member of class-6 family transmembrane semaphorin proteins and acts through Plexin-A1 receptor. It was previously shown that overexpression of SEMA6D in breast cancer cell line MCF-7 leads to a reduction in proliferation and an increase in migration. On the other hand, in the MDA-MB-231 breast cancer cell line, overexpression of SEMA6D had no significant effect on proliferation but enhanced migration. In this study, we aimed to analyze the effects of SEMA6D overexpression in normal breast cell line MCF10A and investigate the invasive behavior and transformation capacity of SEMA6D overexpressing breast cancer cell lines. We demonstrated that overexpression of SEMA6D leads to elevated proliferation, viability and migration in MCF10A cells, whereas it did not trigger their anchorage-independent growth. On the other hand, MDA-MB-231 and MCF7 cells stably expressing SEMA6D showed reduced colony formation in the soft-agar assay. Furthermore, the invasiveness of MDA-MB-231 cells was elevated with SEMA6D overexpression, whereas SEMA6D overexpression did not stimulate the invasiveness of MCF-7 cells through matrigel microenvironment, whereas slightly trigger invasion through bone microenvironment. In conclusion, SEMA6D overexpression has cell-specific effects on breast cancer. The exact role of SEMA6D in breast cancer development remains undefined and must be further investigated.
  • Master Thesis
    Cyr61-Notch Interaction During Epithelial-To Transition, Migration and Invasion in Breast Cancer Cells
    (Izmir Institute of Technology, 2017) İlhan, Mustafa; Yalçın Özuysal, Özden; Yalçın Özuysal, Özden; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of Technology
    Notch signaling is one of the major pathways involved in development and tumorigenesis. Activated Notch is correlated with increased migration, invasion and epithelial-to-mesenchymal-transition (EMT) in breast cancer. However, mechanism of Notch-mediated cancer progression is poorly understood. CYR61 is a secreted protein and its upregulation is also related to increased breast tumorigenesis and EMT. Microarray analyses revealed that CYR61 was differentially expressed in response to Notch activation in breast epithelial cells. We hypothesized that CYR61 is a downstream mediator of Notch during EMT, migration and invasion. To test whether Notch requires CYR61 during EMT, migration and invasion, two complementary approaches were followed: (i) CYR61 expression was silenced by using shRNA in MCF10A epithelial breast cell line in the presence of Notch activation, (ii) CYR61 was over-expressed in MDA-MB-231 cancer breast cell line in the absence of Notch activity. Then, expression of EMT markers was analyzed in mRNA and protein levels via RT-qPCR and immuno-blotting, respectively. Migration and invasion ability of cells were investigated by wound healing assay and a lab-on-a-chip-system, respectively. Here, it was shown that CYR61 inhibition decreased Notch-induced EMT, migration and invasion of MCF10A and CYR61 overexpression in the absence of Notch activity partially rescued Notch-mediated invasion in MDA-MB-231 cell lines. Our findings suggest that CYR61 may act in downstream of Notch and is regulated by Notch. When we consider importance of CYR61 in Notch-induced EMT and cancer progression, targeting CYR61 may hold promise to develop novel strategies for treatment of breast cancer in early stages.