Master Degree / Yüksek Lisans Tezleri

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

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Subject: search.filters.subject.SEMA6D

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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
    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
    Role of Sema6d in Proliferation, Epithelial-Mesenchymal Transition and Migration of Breast Cancer Cell Lines
    (Izmir Institute of Technology, 2017) Şahi, Ece; Yalçın Özuysal, Özden
    Breast cancer is one of the most common cancer types around world and the second leading cause of cancer related deaths among women. Not the primary tumor but distant metastases are mainly the reason of deaths. For metastasis, the cells may go through epithelial-mesenchymal transition (EMT), and acquire migration and invasion abilities. SEMA6D is a transmembrane protein that belongs to a large semaphorin family. SEMA6D is involved in the migration of embryonic cardiac cells. Recently it was validated as an oncogene in osteosarcoma. Also, its oncogenic roles were investigated in gastric cancer and mesothelioma. According to in silico analysis of the Cancer Genome Atlas (TCGA), high SEMA6D expression level is associated with better survival of triple negative breast cancer patients. However, there is not any published study which investigates roles of SEMA6D in breast cancer yet, other than bioinformatic analysis. Therefore, we aimed to understand role of SEMA6D in proliferation, EMT and migration of breast cancer cells. We observed that overexpression of SEMA6D reduces proliferation but enhances migration in non-invasive breast cancer cell line MCF7. Thereby, SEMA6D may increase metastatic ability of MCF7 cells. Its metastatic ability was also supported by changes in EMT markers. On the other hand, proliferation of metastatic breast cancer cell line MDAMB231 was not significantly changed by overexpression of SEMA6D and migration ability was slightly reduced but mesenchymal markers tended to increase in SEMA6D overexpressing MDAMB231 cells. As a conclusion, SEMA6D tends to enhance proliferation, migration through EMT in MCF7 cell line whereas overexpression of SEMA6D did not demonstrate significant effect on metastatic MDA-MB-231 cell line. Therefore, we should separately evaluate role of SEMA6D in different breast cancer cell lines and further studies are required to understand role of SEMA6D in breast cancer.