Researcher:
Özturan, Doğancan

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PhD Student

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Doğancan

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Özturan

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Özturan, Doğancan

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2019 - 201912020 - 20223

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Researcher Of Publications: search.filters.isAuthorOfPublication.701b93f4-b4ba-4ab8-9c79-6d86d7713116

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    Genome-wide ar enhancer activity in prostate cancer
    (American Association for Cancer Research (AACR), 2019) Huang, Flora; Morova, Tunç; Saffarzadeh, Mohammadali; Lack, Nathan Alan; Özturan, Doğancan; PhD Student; Graduate School of Sciences and Engineering; N/A
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    PublicationOpen Access
    Androgen receptor-mediated transcription in prostate cancer
    (Multidisciplinary Digital Publishing Institute (MDPI), 2022) Morova, Tunç; Department of Computer Engineering; Department of Chemical and Biological Engineering; Lack, Nathan Alan; Özturan, Doğancan; Faculty Member; PhD Student; Department of Computer Engineering; Department of Chemical and Biological Engineering; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); School of Medicine; 120842; N/A
    Androgen receptor (AR)-mediated transcription is critical in almost all stages of prostate cancer (PCa) growth and differentiation. This process involves a complex interplay of coregulatory proteins, chromatin remodeling complexes, and other transcription factors that work with AR at cis-regulatory enhancer regions to induce the spatiotemporal transcription of target genes. This enhancer-driven mechanism is remarkably dynamic and undergoes significant alterations during PCa progression. In this review, we discuss the AR mechanism of action in PCa with a focus on how cis-regulatory elements modulate gene expression. We explore emerging evidence of genetic variants that can impact AR regulatory regions and alter gene transcription in PCa. Finally, we highlight several outstanding questions and discuss potential mechanisms of this critical transcription factor.
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    PublicationOpen Access
    Functional mapping of androgen receptor enhancer activity
    (BioMed Central, 2021) Huang, Flora Chia-Chi; Morova, Tunç; Hu, Eugene; Yu, Lok Pak Ivan; Linder, Simon; Hoogstraat, M.; Stelloo, Suzan; Sar, Funda; Van der Poel, Henk; Saffarzadeh, Mohammadali; Le Bihan, Stephane; McConegy, Brian; Y Feng, Felix; Gleave, E. Martin; Bergman, M. Andries; Collins, Colin; Hach, Faraz; Zwart, Wilbert; Emberly, Eldon; N/A; Department of Molecular Biology and Genetics; Özturan, Doğancan; Altıntaş, Umut Berkay; Gökbayrak, Bengül; Lack, Nathan Alan; PhD Student; Faculty Member; Department of Molecular Biology and Genetics; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); Graduate School of Health Sciences; Graduate School of Sciences and Engineering; N/A; N/A; N/A; 120842
    Background: androgen receptor (AR) is critical to the initiation, growth, and progression of prostate cancer. Once activated, the AR binds to cis-regulatory enhancer elements on DNA that drive gene expression. Yet, there are 10-100x more binding sites than differentially expressed genes. It is unclear how or if these excess binding sites impact gene transcription. Results: to characterize the regulatory logic of AR-mediated transcription, we generated a locus-specific map of enhancer activity by functionally testing all common clinical AR binding sites with Self-Transcribing Active Regulatory Regions sequencing (STARRseq). Only 7% of AR binding sites displayed androgen-dependent enhancer activity. Instead, the vast majority of AR binding sites were either inactive or constitutively active enhancers. These annotations strongly correlated with enhancer-associated features of both in vitro cell lines and clinical prostate cancer samples. Evaluating the effect of each enhancer class on transcription, we found that AR-regulated enhancers frequently interact with promoters and form central chromosomal loops that are required for transcription. Somatic mutations of these critical AR-regulated enhancers often impact enhancer activity. Conclusions: using a functional map of AR enhancer activity, we demonstrated that AR-regulated enhancers act as a regulatory hub that increases interactions with other AR binding sites and gene promoters.
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    PublicationOpen Access
    Protein scaffold-based multimerization of soluble ACE2 efficiently blocks SARS-CoV-2 infection in vitro and in vivo
    (Wiley, 2022) Ulbegi Polat, Hivda; Yıldırım, İsmail Selim; Kayabölen, Alişan; Akcan, Uğur; Özturan, Doğancan; Şahin, Gizem Nur; Değirmenci, Nareg Pınarbaşı; Bayraktar, Canan; Söyler, Gizem; Sarayloo, Ehsan; Nurtop, Elif; Özer, Berna; Esken, Gülen Güney; Barlas, Tayfun; Doğan, Özlem; Karahüseyinoğlu, Serçin; Lack, Nathan Alan; Kaya, Mehmet; Albayrak, Cem; Can, Füsun; Solaroğlu, İhsan; Önder, Tuğba Bağcı; PhD Student; PhD Student; Master Student; Faculty Member; Faculty Member; Faculty Member; 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; Koç University Hospital; N/A; N/A; N/A; N/A; N/A; N/A; N/A; N/A; N/A; N/A; N/A; N/A; 170418; 110772; 120842; 10486; N/A; 103165; 102059; 184359
    Soluble ACE2 (sACE2) decoys are promising agents to inhibit SARS-CoV-2, as their efficiency is unlikely to be affected by escape mutations. However, their success is limited by their relatively poor potency. To address this challenge, multimeric sACE2 consisting of SunTag or MoonTag systems is developed. These systems are extremely effective in neutralizing SARS-CoV-2 in pseudoviral systems and in clinical isolates, perform better than the dimeric or trimeric sACE2, and exhibit greater than 100-fold neutralization efficiency, compared to monomeric sACE2. SunTag or MoonTag fused to a more potent sACE2 (v1) achieves a sub-nanomolar IC50, comparable with clinical monoclonal antibodies. Pseudoviruses bearing mutations for variants of concern, including delta and omicron, are also neutralized efficiently with multimeric sACE2. Finally, therapeutic treatment of sACE2(v1)-MoonTag provides protection against SARS-CoV-2 infection in an in vivo mouse model. Therefore, highly potent multimeric sACE2 may offer a promising treatment approach against SARS-CoV-2 infections.