TR Dizin İndeksli Yayınlar / TR Dizin Indexed Publications Collection

Permanent URI for this collectionhttps://hdl.handle.net/11147/7149

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  • Data Paper
    Knockdown of Death Receptor 5 Antisense Long Noncoding Rna and Cisplatin Treatment Modulate Similar Macromolecular and Metabolic Changes in Hela Cells
    (TÜBİTAK - Türkiye Bilimsel ve Teknolojik Araştırma Kurumu, 2022) Gürer, Dilek Cansu; Erdoğan Vatansever, İpek; Ceylan, Çağatay; Akgül, Bünyamin
    Background/aim: Despite great progress in complex gene regulatory mechanisms in the dynamic tumor microenvironment, the potential contribution of long noncoding RNAs (lncRNAs) to cancer cell metabolism is poorly understood. Death receptor 5 antisense (DR5-AS) is a cisplatin inducible lncRNA whose knockdown modulates cell morphology. However, its effect on cell metabolism is unknown. The aim of this study is to examine metabolic changes modulated by cisplatin and DR5-AS lncRNA in HeLa cells. Materials and methods: We used cisplatin as a universal cancer therapeutic drug to modulate metabolic changes in HeLa cervix cancer cells. We then examined the extent of metabolic changes by Fourier transform infrared spectroscopy (FTIR). We also performed transcriptomics analyses by generating new RNA-seq data with total RNAs isolated from cisplatin-treated HeLa cells. Then, we compared cisplatin-mediated transcriptomics and macromolecular changes with those mediated by DR5-AS knockdown. Results: Cisplatin treatment caused changes in the unsaturated fatty acid and lipid-to-protein ratios and the glycogen content. These observations in altered cellular metabolism were supported by transcriptomics analyses. FTIR spectroscopy analyses have revealed that DR5-AS knockdown causes a 20.9% elevation in the lipid/protein ratio and a 76.6% decrease in lipid peroxidation. Furthermore, we detected a 3.42% increase in the chain length of the aliphatic lipids, a higher content of RNA, and a lower amount of glycogen indicating relatively lower metabolic activity in the DR5-AS knockdown HeLa cells. Interestingly, we observed a similar gene expression pattern under cisplatin treatment and DR5-AS knockdown HeLa cells. Conclusion: These results suggest that DR5-AS lncRNA appears to account for a fraction of cisplatin-mediated macromolecular ametabolic changes in HeLa cervix cancer cells.
  • Article
    Citation - WoS: 1
    Citation - Scopus: 2
    Structural and Functional Characterization of Solution, Gel, and Aggregated Forms of Trypsin in Organic Solvent-Assisted and Ph-Induced Phase Changes
    (Türk Biyokimya Derneği, 2015) Ceylan, Çağatay; Karaçiçek, Bilge
    In this study the effect of three different physicochemical parameters on pHtriggered gelation and aggregation of bovine pancreatic trypsin changes and structural and functional changes in these changes in alcohol-water mixtures were studied. Methods: Trypsin gelation times were studied using inverted tube method. Trypsin stability was studied using trypsin enzyme assay. Protein secondary structural changes were monitored using FTIR spectroscopy. Gel and aggregate macrostructures and morphologies were viewed using Scanning Electron Microscopy. Results: The solution phase was observed in the absence of both NaOH and CaCl2. The gel phase was observed in the absence of the either. The aggregate phase was observed in the presence of the both agents all depending on trypsin concentrations used. Trypsin stability studies showed that there were a nearly 53 and 32% specific activity losses after the gelation and aggregation processes. According to FTIR studies β–sheet structure in 1637 cm-1 band disappeared in trypsin gel and trypsin aggregates. Increases in α–helix structure in 1651 cm-1 in trypsin gel and aggregates were observed. Iodoacetamide delayed the gelation and prevented the aggregation indicating the importance of intermolecular disulfides in the both processes. Conclusion: Trypsin gelation was caused by the denaturation of the protein three dimensional structures. The gel and aggregate formation indicates a secondary structural change towards α–helix structure formation at the expense of β–sheet structure and formation of intermolecular disulfide bonds.