Researcher:
Lokumcu, Tolga

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Master Student

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Tolga

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Lokumcu

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Lokumcu, Tolga

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2016 - 20194

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Researcher Of Publications: search.filters.isAuthorOfPublication.da66742b-b35d-4531-9702-7d95fd6d2104

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Now showing 1 - 4 of 4
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    Assessing the function of chromatin modifying enzymes in medulloblastoma
    (Oxford Univ Press Inc, 2016) Oppermann, Udo; N/A; N/A; N/A; Lokumcu, Tolga; Şenbabaoğlu, Fatih; Önder, Tuğba Bağcı; Master Student; Master Student; Faculty Member; Graduate School of Sciences and Engineering; Graduate School of Health Sciences; School of Medicine; N/A; N/A; 184359
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    Examining the role of chromatin modifying enzymes in medulloblastoma by utilizing a chemical library
    (Elsevier, 2016) Oppermann, U.; N/A; N/A; N/A; Lokumcu, Tolga; Şenbabaoğlu, Fatih; Önder, Tuğba Bağcı; Master Student; Master Student; Faculty Member; Graduate School of Sciences and Engineering; Graduate School of Sciences and Engineering; School of Medicine; N/A; N/A; 184359
    N/A
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    PublicationOpen Access
    Engineering human stellate cells for beta cell replacement therapy promotes in vivo recruitment of regulatory T cells
    (Elsevier, 2019) N/A; Department of Chemical and Biological Engineering; Oran, Dilem Ceren; Lokumcu, Tolga; Bal, Tuğba; İnceoğlu, Yasemin; Albayrak, Özgür; Erkan, Murat Mert; Kurtoğlu, Metin; Can, Füsun; Önder, Tuğba Bağcı; Kızılel, Seda; Akolpoğlu, Mükrime Birgül; Faculty Member; Faculty Member; Master Student; Department of Chemical and Biological Engineering; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); Graduate School of Sciences and Engineering; Graduate School of Health Sciences; College of Engineering; School of Medicine; N/A; N/A; N/A; N/A; N/A; N/A; N/A; 103165; 184359; 28376; N/A
    Type 1 diabetes (T1D) is an autoimmune disease characterized by destruction of pancreatic β cells. One of the promising therapeutic approaches in T1D is the transplantation of islets; however, it has serious limitations. To address these limitations, immunotherapeutic strategies have focused on restoring immunologic tolerance, preventing transplanted cell destruction by patients’ own immune system. Macrophage-derived chemokines such as chemokine-ligand-22 (CCL22) can be utilized for regulatory T cell (Treg) recruitment and graft tolerance. Stellate cells (SCs) have various immunomodulatory functions: recruitment of Tregs and induction of T-cell apoptosis. Here, we designed a unique immune-privileged microenvironment around implantable islets through overexpression of CCL22 proteins by SCs. We prepared pseudoislets with insulin-secreting mouse insulinoma-6 (MIN6) cells and human SCs as a model to mimic naive islet morphology. Our results demonstrated that transduced SCs can secrete CCL22 and recruit Tregs toward ​the implantation site in vivo. This study is promising to provide a fundamental understanding of SC-islet interaction and ligand synthesis and transport from SCs at the graft site for ensuring local immune tolerance. Our results also establish a new paradigm for creating tolerable grafts for other chronic diseases such as diabetes, anemia, and central nervous system (CNS) diseases, and advance the science of graft tolerance.
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    PublicationOpen Access
    The pro-apoptotic Bcl-2 family member Harakiri (HRK) induces cell death in glioblastoma multiforme
    (Nature Publishing Group (NPG), 2019) N/A; N/A; Önder, Tuğba Bağcı; Kaya, Ezgi; Cingöz, Ahmet; Şenbabaoğlu, Filiz; Şeker-Polat, Fidan; Sur, İlknur Erdem; Kayabölen, Alişan; Lokumcu, Tolga; Şahin, Gizem Nur; Karahüseyinoğlu, Serçin; Faculty Member; PhD Student; PhD Student; PhD Student; School of Medicine; 184359; N/A; N/A; N/A; N/A; N/A; N/A; N/A; N/A; 110772
    Harakiri (HRK) is a BH3-only protein of the Bcl-2 family and regulates apoptosis by interfering with anti-apoptotic Bcl-2 and Bcl-xL proteins. While its function is mainly characterized in the nervous system, its role in tumors is ill-defined with few studies demonstrating HRK silencing in tumors. In this study, we investigated the role of HRK in the most aggressive primary brain tumor, glioblastoma multiforme (GBM). We showed that HRK is differentially expressed among established GBM cell lines and that HRK overexpression can induce apoptosis in GBM cells at different levels. This phenotype can be blocked by forced expression of Bcl-2 and Bcl-xL, suggesting the functional interaction of Bcl-2/ Bcl-xL and HRK in tumor cells. Moreover, HRK overexpression cooperates with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), a known tumor-specific pro-apoptotic agent. Besides, secondary agents that augment TRAIL response, such as the histone deacetylase inhibitor MS-275, significantly increases HRK expression. In addition, GBM cell response to TRAIL and MS-275 can be partly abolished by HRK silencing. Finally, we showed that HRK induction suppresses tumor growth in orthotopic GBM models in vivo, leading to increased survival. Taken together, our results suggest that HRK expression is associated with GBM cell apoptosis and increasing HRK activity in GBM tumors might offer new therapeutic approaches.