Food Engineering / Gıda Mühendisliği
Permanent URI for this collectionhttps://hdl.handle.net/11147/12
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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, BünyaminBackground/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: 3Citation - Scopus: 4Comparison of the Effects of Statins on A549 Nonsmall-Cell Lung Cancer Cell Line Lipids Using Fourier Transform Infrared Spectroscopy: Rosuvastatin Stands Out(Wiley, 2021) Aksoy, Hatice Nurdan; Ceylan, ÇağatayStatins are commonly prescribed antilipidemic and anticholesterol class of drugs. In addition to their major role, they have been found to have anticancer effects on in vitro, animal and clinical studies. The aim of this study was to investigate the effects of six different statins (rosuvastatin, pravastatin, simvastatin, lovastatin, fluvastatin, and atorvastatin) on A549 cancer cells lipids by Fourier transform infrared (FTIR) spectroscopy. Proliferation tests were carried out to detect the half-maximal inhibitory concentrations (IC50) of each statin on A549 cells. The IC50 values were 50 mu M for simvastatin, 150 mu M for atorvastatin and pravastatin, and 170 mu M for fluvastatin, 200 mu M for rosuvastatin and lovastatin on A549 cells. No correlation was found between the antiproliferative effects of the statins and lipid-lowering effect. The cells were treated with IC5, IC10, and IC50 values of each statins concentration and lipid extracts were compared using FTIR spectroscopy. The results indicated that different statins had different effects on the lipid content of A549 cells. The FTIR spectra of the lipid exctracts of statin-treated A549 cells indicated that the value of hydrocarbon chain length, unsaturation index, oxidative stress level, and phospholipid containing lipids increased except for rosuvastatin-treated A549 cells. In addition, rosuvastatin significantly lowered cholesterol ester levels. In conclusion, the contrasting effects of rosuvastatin should be further investigated.Article 2’-Methylklavuzon Causes Lipid-Lowering Effects on A549 Non-Small Cell Lung Cancer Cells and Significant Changes on Dna Structure Evidenced by Fourier Transform Infrared Spectroscopy(Elsevier, 2020) Ceylan, Çağatay; Aksoy, Hatice Nurdan; Çağır, Ali; Çetinkaya, HakkıVarious chemical agents are used in the treatment of Non-Small Cell Lung Cancer (NSCLC). 2?-methylklavuzon was proposed as a potential chemotherapeutic agent in cancer treatment based on its topoisomerase inhibition activity. In this study the cellular effects of 2?-methylklavuzon was evaluated on A549 cancer cells using FTIR spectroscopy. 2?-methylklavuzon induced significant changes on both the whole cell lyophilizates and the lipid extracts of the A549 lung cancer cells. 2?-methylklavuzon caused significant structural changes in A549 cell DNA structure: T, A and G DNA breathing modes are lost after the drug application indicating the loss of topoisomerase activity. The level of transcription and RNA synthesis was enhanced. 2?-methylklavuzon induced single stranded DNA formation evidenced by the increase in the ratio of asymmetric/symmetric phosphate stretching modes. 2?-methylklavuzon induced band shifts only in the asymmetric mode of phosphate bonds not in the symmetrical phosphate bond stretching. 2?-methylklavuzon induced A form of DNA topography. In addition to the changes in the DNA structure and transcription 2?-methylklavuzon also caused lipid-lowering effect in A549 cancer cells. 2?-methylklavuzon suppressed lipid unsaturation, however, it induced formation of lipids with ring structures. 2?-methylklavuzon suppressed phosphate-containing lipids significantly and decreased carbonyl containing lipids and cholesterol slightly. 2?-methylklavuzon caused increases in the hydrocarbon chain length. Overall, 2?-methylklavuzon can be used as a lipid-lowering compound in the treatment of NSCLC and other cancer therapies. © 2020 Elsevier B.V.Conference Object Antiproliferative and Apoptotic Effects of Ponatinib and Its Effects on Macromolecular Changes in Imatinib-Sensitive and Resistant Chronic Myeloid Leukemia (cml) Cell Lines: a Mechanistic Approach(Ferrata Storti Foundation, 2015) Kartal Yandım, Melis; Ceylan, Çağatay; Elmas, Efe; Baran, Yusuf[No abstract available]Article Citation - WoS: 6Citation - Scopus: 6A Molecular and Biophysical Comparison of Macromolecular Changes in Imatinib-Sensitive and Imatinib-Resistant K562 Cells Exposed To Ponatinib(SAGE Publications Inc., 2016) Kartal Yandım, Melis; Ceylan, Çağatay; Elmas, Efe; Baran, YusufChronic myeloid leukemia (CML) is a type of hematological malignancy that is characterized by the generation of Philadelphia chromosome encoding BCR/ABL oncoprotein. Tyrosine kinase inhibitors (TKIs), imatinib, nilotinib, and dasatinib, are used for the frontline therapy of CML. Development of resistance against these TKIs in the patients bearing T315I mutation is a major obstacle in CML therapy. Ponatinib, the third-generation TKI, is novel drug that is effective even in CML patients with T315I mutation. The exact mechanism of ponatinib in CML has been still unknown. In this study, we aimed to determine the potential mechanisms and structural metabolic changes activated by ponatinib treatment in imatinib-sensitive K562 human CML cell lines and 3 μM-imatinib-resistant K562/IMA3 CML cell lines generated at our lab. Apoptotic and antiproliferative effects of ponatinib on imatinib-sensitive and 3 μM-imatinib-resistant K562/IMA3 CML cells were determined by proliferation and apoptosis assays. Additionally, the effects of ponatinib on macromolecules and lipid profiles were also analyzed using Fourier transform infrared spectroscopy (FTIR). Our results revealed that ponatinib inhibited cell proliferation and induced apoptosis as determined by loss of mitochondrial membrane potential, increased caspase-3 enzyme activity, and transfer of phosphatidylserine to the plasma membrane in both K562 and K562/IMA-3 cells. Furthermore, cell cycle analyses revealed that ponatinib arrested K562 and K562/IMA-3 cells at G1 phase. Moreover, ponatinib treatment created a more ordered nucleic acid structure in the resistant cells. Although the lipid to protein ratio increased in imatinib-sensitive K562 cells with a little decrease in the K562/IMA-3 cells, ponatinib treatment indicated significant changes in the lipid composition such as a significant increase in the cellular cholesterol amounts much more in the K562/IMA-3 cells than the sensitive counterparts. Unsaturation in lipids was higher in the resistant cells; however, increases in lipids without phosphate and the number of acyl chains were much higher in the K562 cells. Taken together, all these results showed powerful antiproliferative and apoptotic effects of ponatinib in both imatinib-sensitive and imatinib-resistant CML cells in a dose-dependent manner, and hence, the use of ponatinib for the treatment of TKI-resistant CML patients may be an effective treatment approach in the clinic. More importantly, these results showed that FTIR spectroscopy can detect drug-induced physiological changes in cancer drug resistance.Article Citation - WoS: 11Citation - Scopus: 9Biophysical Evaluation of Physiological Effects of Gilthead Sea Bream (sparus Aurata) Farming Using Ftir Spectroscopy(Elsevier Ltd., 2014) Ceylan, Çağatay; Tanrıkul, Tansel; Özgener, HüseyinSparus aurata is one of the two most important cultured fish species in the Mediterranean region. The present work investigates the effects of culturing in S. aurata liver tissue at the molecular level using Fourier Transform Infrared (FTIR) spectroscopy. FTIR spectroscopy revealed dramatic differences between the wild and aquacultured fish liver cells, which mainly indicated that the level of glycogen increased in the aquacultured samples and the protein/lipid ratio decreased by 42.29% indicating that triglycerides and cholesterol esters increased and the protein content decreased in the aquacultured samples. The 15.99% increase in the level of unsaturation indicated elevated lipid peroxidation. Structural/organisational changes in the nucleic acids along with increased transcriptional status of the liver tissue cells were observed in the cultured fish tissue. All these results indicated that culturing induces significant changes in fish physiology. In addition FTIR spectroscopy is a promising method to monitor the physiological changes in fish physiology.Article Citation - WoS: 11Citation - Scopus: 9Quantification of Staphylococcus Aureus in White Cheese by the Improved Dna Extraction Strategy Combined With Taqman and Lna Probe-Based Qpcr(Elsevier Ltd., 2014) Kadiroğlu, Pınar; Korel, Figen; Ceylan, ÇağatayFour different bacterial DNA extraction strategies and two different qPCR probe chemistries were studied for detection of Stapylococcus aureus from white cheeses. Method employing trypsin treatment followed by a commercial kit application and TaqMan probe-based qPCR was the most sensitive one detecting higher counts than standards in naturally contaminated samples.Article Citation - WoS: 13Citation - Scopus: 13Macromolecular Changes in Nilotinib Resistant K562 Cells; an in Vitro Study by Fourier Transform Infrared Spectroscopy(SAGE Publications Inc., 2012) Ceylan, Çağatay; Camgöz, Aylin; Baran, YusufNilotinib is a second generation tyrosine kinase inhibitor which is used in both first and second line treatment of chronic myeloid leukemia (CML). In the present work, the effects of nilotinib resistance on K562 cells were investigated at the molecular level using Fourier transform infrared (FT-IR) spectroscopy. Human K562 CML cells were exposed to step-wise increasing concentrations of nilotinib, and sub-clones of K562 cells resistant to 50 nM nilotinib were generated and referred to as K562/NIL-50 cells. Antiproliferative effects of nilotinib were determined by XTT cell proliferation assay. Changes in macromolecules in parental and resistant cells were studied by FT-IR spectroscopy. Nilotinib resistance caused significant changes which indicated increases in the level of glycogen and membrane/lipid order. The amount of unsaturated lipids increased in the nilotinib resistant cells indicating lipid peroxidation. The total amount of lipids did not change significantly but the relative proportion of cholesterol and triglycerides altered considerably. Moreover, the transcriptional status decreased but metabolic turn-over increased as revealed by the FT-IR spectra. In addition, changes in the proteome and structural changes in both proteins and the nucleus were observed in the K562/NIL-50 cells. Protein secondary structural analyses revealed that alpha helix structure and random coil structure decreased, however, anti-parallel beta sheet structure, beta sheet structure and turns structure increased. These results indicate that the FT-IR technique provides a method for analyzing drug resistance related structural changes in leukemia and other cancer types.Article Citation - WoS: 1Citation - Scopus: 2Structural 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, BilgeIn 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.Article Citation - WoS: 16Citation - Scopus: 15The Roles of Macromolecules in Imatinib Resistance of Chronic Myeloid Leukemia Cells by Fourier Transform Infrared Spectroscopy(Elsevier Ltd., 2013) Baran, Yusuf; Ceylan, Çağatay; Camgöz, AylinImatinib is a first generation tyrosine kinase inhibitor, which is used for the treatment of chronic myeloid leukemia. However, resistance to imatinib is an important problem. Different mechanisms have been explained for imatinib resistance. In this study, we examined the roles of macromolecules in imatinib resistance in K562 cells at the molecular level using Fourier Transform Infrared (FT-IR) spectroscopy. An amount of 3μM imatinib resistant cells were generated by our group and named as K562/IMA-3 cells. Changes in macromolecules in parental and resistant cells were studied by FT-IR spectroscopy. Imatinib resistance caused changes, which indicated decreases in the level of glycogen and increases in the membrane order. The amount of unsaturated lipids increased in the imatinib resistant cells indicating lipid peroxidation. Imatinib resistance caused changes in the lipid/protein ratio. The relative protein content increased with respect to nucleic acids indicating higher transcription and protein expression and structural/organizational changes in the nucleus were evident as revealed by frequency changes in the nucleic acid bands. Changes in the amide bands revealed changes in the proteome of the resistant cells. Protein secondary structural changes indicated that the antiparallel beta sheet's structure increased, however the alpha helix structure, beta sheet structure, random coil structure and turns decreased in the resistant cells. These results indicate that the FT-IR technique provides a suitable method for analyzing drug resistance related structural changes in leukemia and other cancer types.