Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection

Permanent URI for this collectionhttps://hdl.handle.net/11147/7148

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Author: search.filters.author.Akgül, BünyaminDepartment: search.filters.department.Izmir Institute of Technology

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  • Review
    Citation - WoS: 4
    Citation - Scopus: 4
    Unraveling the Intriguing Interplay: Exploring the Role of Lncrnas in Caspase-Independent Cell Death
    (Wiley, 2024) Akgül, Bünyamin; Erdoğan, İpek; Vatansever, Ipek Erdogan; Akgul, Buenyamin; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of Technology
    Cell death plays a crucial role in various physiological and pathological processes. Until recently, programmed cell death was mainly attributed to caspase-dependent apoptosis. However, emerging evidence suggests that caspase-independent cell death (CICD) mechanisms also contribute significantly to cellular demise. We and others have reported and functionally characterized numerous long noncoding RNAs (lncRNAs) that modulate caspase-dependent apoptotic pathways potentially in a pathway-dependent manner. However, the interplay between lncRNAs and CICD pathways has not been comprehensively documented. One major reason for this is that most CICD pathways have been recently discovered with some being partially characterized at the molecular level. In this review, we discuss the emerging evidence that implicates specific lncRNAs in the regulation and execution of CICD. We summarize the diverse mechanisms through which lncRNAs modulate different forms of CICD, including ferroptosis, necroptosis, cuproptosis, and others. Furthermore, we highlight the intricate regulatory networks involving lncRNAs, protein-coding genes, and signaling pathways that orchestrate CICD in health and disease. Understanding the molecular mechanisms and functional implications of lncRNAs in CICD may unravel novel therapeutic targets and diagnostic tools for various diseases, paving the way for innovative strategies in disease management and personalized medicine.
  • Article
    Citation - WoS: 4
    Citation - Scopus: 3
    Expression Patterns of M6a Rna Methylation Regulators Under Apoptotic Conditions in Various Human Cancer Cell Lines
    (TUBITAK, 2024) Akgül, Bünyamin; Sağlam, Buket; Vatansever, İpek Erdoğan; Akgül, Bünyamin; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of Technology
    Background/aim: Cancer is a complex disease that involves both genetic and epigenetic factors. While emerging evidence clearly suggests that changes in epitranscriptomics play a crucial role in cancer pathogenesis, a comprehensive understanding of the writers, erasers, and readers of epitranscriptomic processes, particularly under apoptotic conditions remains lacking. The aim of this study was to uncover the changes in the expression of m6A RNA modifiers under apoptotic conditions across various cancer cell lines. Materials and methods: Initially, we quantified the abundance of m6A RNA modifiers in cervical (HeLa and ME180), breast (MCF7 and MDA-MB-231), lung (A549 and H1299), and colon (Caco-2 and HCT116) cancer cell lines using qPCR. Subsequently, we induced apoptosis using cisplatin and tumor necrosis factor-alpha (TNF-α) to activate intrinsic and extrinsic pathways, respectively, and assessed apoptosis rates via flow cytometry. Further, we examined the transcript abundance of m6A RNA modifiers under apoptotic conditions in cervical, breast, and lung cancer cell lines using qPCR. Results: Overall, treatment with cisplatin increased the abundance of m 6A modifiers, whereas TNF-α treatment decreased their expression in cervical, breast, and lung cancer cell lines. Specifically, cisplatin-induced apoptosis, but not TNF-α-mediated apoptosis, resulted in decreased abundance of METTL14 and FTO transcripts. Additionally, cisplatin treatment drastically reduced the abundance of IGF2BP2 and IGF2BP3 readers. Conclusion: These results suggest that the differential response of cancer cells to apoptotic inducers may be partially attributed to the expression of m6A RNA modifiers.