Researcher:
Önder, Tuğba Bağcı

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Tuğba Bağcı

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Önder

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Önder, Tuğba Bağcı

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2013 - 2019272020 - 202320

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Researcher Of Publications: search.filters.isAuthorOfPublication.10081304-6705-42bd-a174-9fe6bf3520d5

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Now showing 1 - 10 of 47
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    Investigation of ionizing radiation response in new resistance models of glioblastoma.
    (Amer Assoc Cancer Research, 2021) N/A; N/A; Değirmenci, Nareg Pınarbaşı; Önder, Tuğba Bağcı; Sur, İlknur Erdem; Selek, Uğur; PhD Student; Faculty Member; Faculty Member; Faculty Member; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); Graduate School of Health Sciences; School of Medicine; School of Medicine; School of Medicine; N/A; 184359; N/A; 27211
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    Epigenetic modifications of androgen receptor signaling in castration resistant prostate cancer (CRPC)
    (Elsevier Sci Ltd, 2014) Saraç, Hilal; Toparlak, Ömer Duhan; Kaplan, Anıl; Ebrahimi, Ayyub A.; Önder, Tuğba Bağcı; Önder, Tamer Tevfik; Lack, Nathan Alan; PhD Student; Other; Undergraduate Student; Researcher; Faculty Member; Faculty Member; Faculty Member; Graduate School of Sciences and Engineering; School of Medicine; School of Medicine; School of Medicine; School of Medicine; School of Medicine; School of Medicine; N/A; N/A; N/A; 381072; 184359; 42946; 120842
    Introduction: Prostate cancer is one of the most common forms of cancer in Turkish and European men. For those patients with late-stage prostate cancer, androgen depletion therapy is current standard treatment. While initially successful, almost all patients eventually develop resistance against this treatment. Once the cancer reaches this advanced, progressive form, it is termed castration resistant prostate cancer (CRPC). Whereas the progression mechanisms of CRPC are poorly understood, it has been shown that in CRPC patients, the androgen receptor (AR) is still active despite undetectable androgen levels. Since AR signaling is important in the progression and growth of prostate cancer, understanding how AR mediated signaling occurs in CRPC is critical to more efficient treatment of this recurrent disease. Material and Methods: There are several possible causes for this conversion from androgen-sensitive to androgen-independent prostate cancer. Previous work has demonstrated that epigenetic modifiers such as EZH2 and LSD1 can mediate the sensitization of androgen receptor in CRPC. However, only a small subset of epigenetic modifiers has been characterized. To better understand the role of histone modification on CRPC, we conducted a large scale shRNA screen of epigenetic modifying enzymes to identify those genes that prevent androgen-independent growth. Results and Discussion: From this screen several hit genes have been found that cause a reversion of androgen-independent to androgen-dependent prostate cancer. The shRNA knock-down of these hit genes was confirmed by western blot and qRT-PCR. We are currently characterizing how these epigenetic modifiers affect androgen-receptor mediated signalling. Conclusion: These results will offer new insight into the role of epigenetic modifiers in nuclear receptor signalling.
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    Directing chemiluminescent dioxetanes to mitochondria: a cationic luminophore enables in vitro and in vivo detection of cancer cells upon enzymatic activation
    (Elsevier B.V., 2023) Department of Chemistry; N/A; N/A; Department of Chemistry; N/A; N/A; N/A; N/A; N/A; Department of Chemistry; Gündüz, Hande; Acari, Alperen; Çetin, Sultan; Almammadov, Toghrul; Değirmenci, Nareg Pınarbaşı; Dırak, Musa; Cingöz, Ahmet; Kılıç, Eda; Önder, Tuğba Bağcı; Kölemen, Safacan; Researcher; Master Student; PhD Student; Researcher; PhD Student; PhD Student; Researcher; Master Student; Faculty Member; Faculty Member; Department of Chemistry; N/A; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); N/A; N/A; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); N/A; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); N/A; N/A; N/A; College of Sciences; Graduate School of Health Sciences; Graduate School of Sciences and Engineering; College of Sciences; Graduate School of Health Sciences; Graduate School of Sciences and Engineering; N/A; Graduate School of Sciences and Engineering; School of Medicine; College of Sciences; 224496; N/A; N/A; N/A; N/A; N/A; N/A; N/A; 184359; 272051
    A mitochondrion targeted and leucine aminopeptidase (LAP) activatable 1,2-dioxatane based chemiluminescent probe (MCL) for detection of LAP activity in living cancer cells and tumor bearing mice was reported. MCL displayed a selective and sensitive turn-on response in aqueous solutions upon reacting with the LAP enzyme. In cell culture studies, a selective luminescence intensity increase was observed in cancer cell lines, suggesting that MCL can differentiate between cancer and normal cells and allows detection of varying endogenous LAP concentrations. Using fluorescence imaging with a commercial Mitotracker dye, MCL was also shown to localize mitochondria in cancer cell lines. Furthermore, MCL was used to image tumors in mice models. MCL marks not only the first ever example of a mitochondria targeted chemiluminescent probe, but also the first ever example of an organelle targeted 1,2-dioxetane derivative. © 2023 Elsevier B.V.
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    Assessment of the MRI and behavioral test results in a focal cerebral ischemia-reperfusion model in the rat after separate and combined use of mouse-derived neural progenitor cells, human-derived neural progenitor cells and atorvastatin
    (Turkish Neurosurgical Soc, 2018) Tanta, Alican; Izgi, Nail; Erdag, Ece; Aras, Yavuz; Genc, Cetin; N/A; Önder, Tuğba Bağcı; Faculty Member; School of Medicine; 184359
    AIM: To assess the efficacy of Neural progenitor cell (NPC) transplantation in ischemic stroke, and to investigate whether atorvastatin enhances therapeutic potency of NPC after stroke. MATERIAL and METHODS: The focal cerebral ischemia-reperfusion model was performed by transient occlusion of middle cerebral artery. Rats were assigned randomly to receive intracerebral transplantation of mouse NPC alone (mNPC), human NPC alone (hNPC), mouse NPC plus oral atorvastatin (mNPC+A), human NPC plus oral atorvastatin (hNPC+A), oral atorvastatin alone, or intracerebral Dulbecco's Modified Eagle's medium injection (control group). Adhesive removal, rotarod, cylinder tests, and magnetic resonance imaging (MRI) were used for assessment of rats during 4 weeks. After sacrification on 28th day, rats were investigated by immunofluorescent staining. RESULTS: The hNPC and mNPC groups showed significantly improved functional outcome and reduced infarct area ratio compared with the control group. The hNPC group had significantly better performance and lower infarct area ratio than the mNPC group. Addition of atorvastatin to stem cell therapy significantly improved functional outcome, although it did not affect the infarct area ratio on MRI. Anti-inflammatory response in the infarct area was higher in the mNPC group. NPC transplantation significantly reduced the amount of microglia and a significant increase in the amount of astrocytes. CD8a+ T lymphocyte and granzyme B activities were not detected in any of the subjects. CONCLUSION: Both hNPC and mNPC treatments significantly improved functional outcome, and reduced infarct area ratio after stroke. Atorvastatin enhanced the therapeutic potency of NPCs, including neurological improvement.
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    A platinum blue complex exerts its cytotoxic activity via DNA damage and induces apoptosis in cancer cells
    (Wiley, 2017) Adiguzel, Zelal; Ozalp-Yaman, Seniz; Celik, Gokalp; Salem, Safia; Cetin, Yuksel; Acilan, Ceyda; N/A; N/A; Önder, Tuğba Bağcı; Şenbabaoğlu, Filiz; Faculty Member; PhD Student; School of Medicine; Graduate School of Health Sciences; 184359; N/A
    Here, we describe the characteristics of a Pt-blue complex [Pt-4(2-atp)(8)(H2O)(OH)] (2-atp: 2-aminothiophenol) as a prodrug for its DNA-binding properties and its use in cancer therapy. The nature of the interaction between the Pt-blue complex and DNA was evaluated based on spectroscopic measurements, the electronic absorption spectra, thermal behavior, viscosity, fluorometric titration, and agarose gel electrophoresis. Our results suggested that the compound was able to partially intercalate DNA and appeared to induce both single- and double-stranded breaks (DBS) on DNA in vitro, but no DSBs in cells. The ability of the compound to induce DNA damage was dependent on reactive oxygen species (ROS) in vitro. There was also elevated formation of ROS and SOD expression in response to drug treatment in cell culture. The complex was found to be more cytotoxic to cancer cells in comparison with noncancer controls using WST-1 assay. The mean of cell death was determined to be apoptosis as assessed via biochemical, morphological, and molecular observations, including DNA condensation/fragmentation analysis, live cell imaging microscopy, TUNEL analyses, and increase in the levels of pro-apoptotic genes such as Bag3, Bak, Bik, Bmf, and Hrk. Hence, the Pt-blue complex under study grants premise for further studies.
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    Changes on the expression of 84 key genes involved in the progression of hepatocellular carcinoma (HCC) during differentiation of HepG2 cells
    (Amer Soc Cell Biology, 2013) Aktaş, Ranan Gülhan; Önder, Tuğba Bağcı; Faculty Member; School of Medicine; 184359
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    Identification of novel molecular players of GBM cell dispersal through an in vitro profiling approach
    (Oxford Univ Press, 2016) Gümüş, Zeynep Hülya; N/A; N/A; N/A; N/A; Department of Industrial Engineering; N/A; Şeker-Polat, Fidan; Erkent, Mahmut Alp; Ergüder, Nazlı; Sevinç, Kenan; Gönen, Mehmet; Önder, Tuğba Bağcı; Phd Student; Undergraduate Student; Undergraduate Student; Phd Student; Faculty Member; Faculty Member; Department of Industrial Engineering; Graduate School of Health Sciences; School of Medicine; School of Medicine; Graduate School of Sciences and Engineering; College of Engineering; School of Medicine; N/A; N/A; N/A; N/A; 237468; 184359
    Glioblastoma multiforme (GBM) is the most common and aggressive type of gliomas with a mean survival of 1 year after diagnosis. A major obstacle in treating GBMs is extensive tumor cell infiltration into the surrounding brain. Despite tumor resection and combined therapy, recurrence occurs in the vicinity of the resection margin due to individual cells that dispersed out of the primary tumor, therefore; developing novel therapies that target tumor cell dispersal is of high priority. The goal of this project is to identify genes that are differentially regulated during GBM cell dispersal and to validate their function in in vitro models of dispersal. In this project, we have used an in vitro model of cell motility whereby the dynamics of GBM cell dispersal can be monitored in real-time and quantitated. Accordingly, we isolated motile/migratory/dispersive cells from non-motile/core cells and used these cells for investigating the genes that are differentially regulated during different phases of cell movement by using RNA sequencing. Analysis of the sequencing experiments showed the presence of many differentially expressed genes in motile vs non-motile cells. Most of the genes that have the highest expression in motile cells compared to non-motile ones were linked to epithelial to mesenchymal transition and cell motility based on our pathway and gene set enrichment analyses. Our current focus is on five different candidate genes: CTGF, CYR61, SERPINE1, INHBA and PTX3. Among these, the expression of SERPINE1, a serine protease inhibitor, had predictive value for overall survival of gliomas and therefore is an interesting therapeutic candidate. Currently, we are conducting loss-of-function and gain-of function experiments targeting these genes. Together, these studies have the potential to discover novel molecular players of GBM cell dispersal and open up new avenues for designing new therapeutic strategies against the invasive phenotype of otherwise untreatable malignant GBMs.
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    Mitoxantrone potentiates TRAIL-induced apoptosis in glioblastoma multiforme
    (Oxford Univ Press, 2016) Ayhan, Ceyda Açılan; N/A; N/A; N/A; Department of Molecular Biology and Genetics; N/A; N/A; Şenbabaoğlu, Filiz; Cingöz, Ahmet; Kaya, Ezgi; Kazancıoğlu, Selena; Lack, Nathan Alan; Önder, Tuğba Bağcı; PhD Student; Researcher; PhD Student; Undergraduate Student; Faculty Member; Faculty Member; Department of Molecular Biology and Genetics; Graduate School of Health Sciences; Graduate School of Health Sciences; Graduate School of Health Sciences; College of Sciences; School of Medicine; School of Medicine; N/A; N/A; N/A; N/A; 120842; 184359
    Glioblastoma multiforme (GBM) is the most aggressive and frequent type of primary brain tumor with dismal survival rates. As GBM cells suppress apoptosis and evade death, re-activating dormant apoptotic programs with pro-apoptotic ligands or small molecules might be a promising approach. As such, the tumor-selective killing capacity of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a potential treatment option in GBM. However, many tumor cells are intrinsically resistant and/or acquire resistance to TRAIL. In this study, we conducted an extensive drug-re-profiling screen to identify FDA-approved compounds that can be used clinically as TRAIL-sensitizing agents in GBM. Using selected isogenic GBM cell pairs with differential levels of TRAIL sensitivity, we revealed 26 TRAIL-sensitizing compounds, 13 of which were effective as single agents. One drug, Mitoxantrone, a DNA-damaging agent, did not cause toxicity to non-malignant cells at the doses that synergized with TRAIL on tumor cells. We investigated the downstream changes in apoptosis pathway components upon Mitoxantrone treatment, and observed that Death Receptors (DR4 and DR5) expression was upregulated, and pro-apoptotic and anti-apoptotic gene expression patterns were altered in favor of apoptosis. Together, our results suggest that combination of Mitoxantrone and TRAIL can be a promising therapeutic approach for GBM patients.
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    Derivation of neural stem cells from mouse induced pluripotent stem cells
    (Humana Press Inc, 2016) N/A; N/A; Karanfil, Işıl; Önder, Tuğba Bağcı; Undergraduate Student; Faculty Member; School of Medicine; School of Medicine; N/A; 184359
    Neural stem cells (NSCs) derived from induced pluripotent stem cells offer therapeutic tools for neurodegenerative diseases. This review focuses on embryoid body (EB)-mediated stem cell culture techniques used to derive NSCs from mouse induced pluripotent stem cells (iPSCs). Generation of healthy and stable NSCs from iPSCs heavily depends on standardized in vitro cell culture systems that mimic the embryonic environments utilized during neural development. Specifically, the neural induction and expansion methods after EB formation are described in this review.
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    Quinacrine mediated sensitization of glioblastoma (GBM) cells to TRAIL through MMP-sensitive PEG hydrogel carriers
    (Wiley-V C H Verlag Gmbh, 2017) N/A; N/A; N/A; Department of Chemical and Biological Engineering; Erkoç, Pelin; Cingöz, Ahmet; Önder, Tuğba Bağcı; Kızılel, Seda; PhD Student; Researcher; Faculty Membe; Faculty Member; Department of Chemical and Biological Engineering; Graduate School of Sciences and Engineering; Graduate School of Health Sciences; School of Medicine; College of Engineering; N/A; N/A; 184359; 28376
    Overcoming drug resistance is a major challenge for cancer therapy. Tumor necrosis factor alpha-related apoptosis-inducing ligand (TRAIL) is a potent therapeutic as an activator of apoptosis, particularly in tumor but not in healthy cells. However, its efficacy is limited by the resistance of tumor cell populations to the therapeutic substance. Here, we have addressed this limitation through the development of a controlled release system, matrix-metalloproteinase (MMP)-sensitive and arg-gly-asp-ser (RGDS) peptide functionalized poly (ethylene-glycol) (PEG) particles which are synthesized via visible-light-induced water-in-water emulsion polymerization. Quinacrine (QC), a recently discovered TRAIL sensitizer drug, is loaded into the hydrogel carriers and the influence of this system on the apoptosis of a malignant type of brain cancer, glioblastoma multiforme (GBM), has been investigated in detail. The results suggest that MMP-sensitive particles are cytocompatible and superior to promote TRAIL-induced apoptosis in GBM cells when loaded with QC. Compared to QC and TRAIL alone, combination of QC-loaded PEG hydrogel and TRAIL demonstrates synergistic apoptotic inducing behavior. Furthermore, QC-loaded particles, but not QC or PEG-hydrogels alone, enhance apoptosis as is measured through expression of apoptosis-related genes. This system is promising to significantly improve the efficacy of chemotherapeutic drugs and suggests a combination treatment for GBM therapy.