Food Engineering / Gıda Mühendisliği

Permanent URI for this collectionhttps://hdl.handle.net/11147/12

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Start date: 2010Department: search.filters.department.İzmir Institute of Technology. Molecular Biology and Genetics

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Now showing 1 - 5 of 5
  • 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) Akgül, Bünyamin; Ceylan, Çağatay; Erdoğan, İpek; Akgül, Bünyamin; 04.03. Department of Molecular Biology and Genetics; 03.08. Department of Food Engineering; 03. Faculty of Engineering; 04. Faculty of Science; 01. Izmir Institute of Technology
    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.
  • 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; Ceylan, Çağatay; Baran, Yusuf; Elmas, Efe; Baran, Yusuf; 04.03. Department of Molecular Biology and Genetics; 03.08. Department of Food Engineering; 03. Faculty of Engineering; 04. Faculty of Science; 01. Izmir Institute of Technology
    [No abstract available]
  • Article
    Citation - WoS: 6
    Citation - Scopus: 6
    A 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; Baran, Yusuf; Baran, Yusuf; Ceylan, Çağatay; 04.03. Department of Molecular Biology and Genetics; 03.08. Department of Food Engineering; 03. Faculty of Engineering; 04. Faculty of Science; 01. Izmir Institute of Technology
    Chronic 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: 16
    Citation - Scopus: 15
    The Roles of Macromolecules in Imatinib Resistance of Chronic Myeloid Leukemia Cells by Fourier Transform Infrared Spectroscopy
    (Elsevier Ltd., 2013) Baran, Yusuf; Ceylan, Çağatay; Baran, Yusuf; Ceylan, Çağatay; 04.03. Department of Molecular Biology and Genetics; 03.08. Department of Food Engineering; 03. Faculty of Engineering; 04. Faculty of Science; 01. Izmir Institute of Technology
    Imatinib 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.
  • Article
    Citation - WoS: 111
    Citation - Scopus: 124
    Salt Tolerance in Solanum Pennellii: Antioxidant Response and Related Qtl
    (BioMed Central Ltd., 2010) Frary, Anne; Göl, Deniz; Frary, Anne; Ökmen, Bilal; Pınar, Hasan; Ökmen, Bilal; Yemenicioğlu, Ahmet; Doğanlar, Sami; Yemenicioğlu, Ahmet; Doğanlar, Sami; 04.03. Department of Molecular Biology and Genetics; 03.01. Department of Bioengineering; 03.08. Department of Food Engineering; 03. Faculty of Engineering; 04. Faculty of Science; 01. Izmir Institute of Technology
    Background: Excessive soil salinity is an important problem for agriculture, however, salt tolerance is a complex trait that is not easily bred into plants. Exposure of cultivated tomato to salt stress has been reported to result in increased antioxidant content and activity. Salt tolerance of the related wild species, Solanum pennellii, has also been associated with similar changes in antioxidants. In this work, S. lycopersicum M82, S. pennellii LA716 and a S. pennellii introgression line (IL) population were evaluated for growth and their levels of antioxidant activity (total water-soluble antioxidant activity), major antioxidant compounds (phenolic and flavonoid contents) and antioxidant enzyme activities (superoxide dismutase, catalase, ascorbate peroxidase and peroxidase) under both control and salt stress (150 mM NaCl) conditions. These data were then used to identify quantitative trait loci (QTL) responsible for controlling the antioxidant parameters under both stress and nonstress conditions.Results: Under control conditions, cultivated tomato had higher levels of all antioxidants (except superoxide dismutase) than S. pennellii. However, under salt stress, the wild species showed greater induction of all antioxidants except peroxidase. The ILs showed diverse responses to salinity and proved very useful for the identification of QTL. Thus, 125 loci for antioxidant content under control and salt conditions were detected. Eleven of the total antioxidant activity and phenolic content QTL matched loci identified in an independent study using the same population, thereby reinforcing the validity of the loci. In addition, the growth responses of the ILs were evaluated to identify lines with favorable growth and antioxidant profiles.Conclusions: Plants have a complex antioxidant response when placed under salt stress. Some loci control antioxidant content under all conditions while others are responsible for antioxidant content only under saline or nonsaline conditions. The localization of QTL for these traits and the identification of lines with specific antioxidant and growth responses may be useful for breeding potentially salt tolerant tomato cultivars having higher antioxidant levels under nonstress and salt stress conditions.