Researcher:
Urman, Defne

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Defne

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Urman

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Urman, Defne

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2016 - 20184

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Researcher Of Publications: search.filters.isAuthorOfPublication.06724544-eef0-45ee-85d7-5762de6d54ef

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    The expressions of ovarian steroidogenic enzymes do not increase proportionally after FSH, creating a shunting that promotes progesterone output in the granulosa cells without luteinization
    (Oxford University Press (OUP), 2016) Seyhan, A.; Keles, I.; Balaban, B.; N/A; N/A; N/A; N/A; Akın, Nazlı; Bildik, Gamze; Urman, Defne; Urman, Cumhur Bülent; Öktem, Özgür; Master Student; Teaching Faculty; Master Student; N/A; Faculty Member; Faculty Member; Graduate School of Health Sciences; School of Medicine; Graduate School of Health Sciences; N/A; School of Medicine; School of Medicine; N/A; N/A; N/A; N/A; 12147; 102627
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    Imatinib mesylate accelerates follicle death andis not protective against chemotherapy induced damage in human ovary
    (Elsevier Science Inc, 2016) Keles, I.; Balaban, B.; Bildik, Gamze; Akın, Nazlı; Urman, Defne; Urman, Cumhur Bülent; Öktem, Özgür; Teaching Faculty; Master Student; Researcher; Faculty Member; Faculty Member; School of Medicine; Graduate School of Health Sciences; Graduate School of Health Sciences; School of Medicine; School of Medicine; N/A; N/A; N/A; 12147; 102627
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    Cytotoxicity and mitogenicity assays with real-time and label-free monitoring of human granulosa cells with an impedance-based signal processing technology intergrating micro-electronics and cell biology
    (Pergamon-Elsevier Science Ltd, 2016) Yakar, Feridun; Güzel, Yılmaz; Balaban, Başak; Iwase, Akira; N/A; Öktem, Özgür; Bildik, Gamze; Şenbabaoğlu, Filiz; Lack, Nathan Alan; Akın, Nazlı; Urman, Defne; Urman, Cumhur Bülent; Faculty Member; Teaching Faculty; PhD Student; Faculty Member; Master Student; Master Student; Faculty Member; School of Medicine; School of Medicine; Graduate School of Health Sciences; School of Medicine; Graduate School of Health Sciences; Graduate School of Health Sciences; School of Medicine; 102627; N/A; N/A; 120842; N/A; N/A; 12147
    A recently developed technology (xCelligence) integrating micro-electronics and cell biology allows real-time, uninterrupted and quantitative analysis of cell proliferation, viability and cytotoxicity by measuring the electrical impedance of the cell population in the wells without using any labeling agent. In this study we investigated if this system is a suitable model to analyze the effects of mitogenic (FSH) and cytotoxic (chemotherapy) agents with different toxicity profiles on human granulosa cells in comparison to conventional methods of assessing cell viability, DNA damage, apoptosis and steroidogenesis. The system generated the real-time growth curves of the cells, and determined their doubling times, mean cell indices and generated dose-response curves after exposure to cytotoxic and mitogenic stimuli. It accurately predicted the gonadotoxicity of the drugs and distinguished less toxic agents (5-FU and paclitaxel) from more toxic ones (cisplatin and cyclophosphamide). This platform can be a useful tool for specific end-point assays in reproductive toxicology.
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    PublicationOpen Access
    Endogenous c-Jun N-terminal kinase (JNK) activity marks the boundary between normal and malignant granulosa cells
    (Nature Publishing Group (NPG), 2018) İnce, Ümit; Palaoğlu, Erhan; Arvas, Macit; Güzel, Yılmaz; N/A; Bildik, Gamze; Akın, Nazlı; Şenbabaoğlu, Filiz; Esmaeilian, Yashar; Şahin, Gizem Nur; Urman, Defne; Karahüseyinoğlu, Serçin; Taşkıran, Çağatay; Yakın, Kayhan; Öktem, Özgür; Teaching Faculty; Master Student; PhD Student; PhD Student; Faculty Member; Faculty Member; Faculty Member; Faculty Member; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); School of Medicine; Graduate School of Health Sciences; N/A; N/A; N/A; N/A; N/A; N/A; 110772; N/A; N/A; 102627
    Granulosa cell tumor of the ovary (GCT) is a very rare tumor, accounting for only 2% of all ovarian tumors. It originates from sex cords in the ovary and can be divided into adult (95%) and juvenile (5%) types based on histologic findings. To date, no clear etiologic process has been identified other than a missense point mutation in the FOXL2 gene. Our previous works showed that c-Jun N-terminal kinase (JNK) pathway plays critical role in cell cycle progression and mitosis of normal and immortalized granulosa cells and follicle growth in rodent ovaries. These findings led us to investigate the role of JNK pathway in the granulosa cell tumor of the ovary. We used two different GCT cell lines (COV434 and KGN) and fresh GCT samples of adult and juvenile types obtained from the patients during surgery. We have discovered that endogenous kinase activity of JNK is markedly enhanced in the GCT samples and cell lines, whereas it was almost undetectable in mitotic non-malignant human granulosa cells. The inhibition of JNK pathway in GCT cell lines with two different pharmacologic inhibitors (SP600125 and AS601245) or siRNA resulted in a dose-dependent reduction in in vitro cell growth, increased apoptosis and diminished estradiol and AMH productions. JNK inhibition was also associated with a decrease in the number of cells positive for mitosis marker phospho-histone H3(Ser) 10 in the asynchronous cells; and diminished EdU uptake during S phase and cell cycle arrest at G2/M-phase transition in the synchronized cells. Ex vivo treatment of patient-derived GCT samples with JNK inhibitors for 24 h significantly decreased their in vitro growth and estradiol and AMH productions. Furthermore, in human GCT xenograft model, in vivo tumor growth was significantly reduced and plasma AMH levels were significantly decreased in SCID mice after administration of JNK inhibitors and siRNA. These findings suggest that targeting JNK pathway may provide therapeutic benefit in the treatment of granulosa cell tumors for which currently no curative therapy exists beyond surgery.