Investigation into drug resistance to cisplatin in cancer stem cell-enriched population in non-small cell lung cancer

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dc.authorscopusidEngin Ulukaya / 6602927353
dc.authorwosidEngin Ulukaya / KYY-4020-2024
dc.contributor.authorDere, Egemen
dc.contributor.authorAkgün, Oǧuzhan
dc.contributor.authorAztopal, Nazllhan
dc.contributor.authorUlukaya, Engin
dc.date.accessioned2025-04-18T10:55:21Z
dc.date.available2025-04-18T10:55:21Z
dc.date.issued2025
dc.departmentİstinye Üniversitesi, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü
dc.description.abstractunderstanding drug resistance in cancer is of importance in treatment. Cancer stem cells are main factor for drug resistance. Therefore, the possible gene/gene interactions/proteins were explored in our study using a cancer stem cell-enriched population (H1299/S) derived from a parental non-small cell lung cancer cell line (H1299/P). response to cisplatin, which is the main drug for the treatment of lung cancer, was evaluated with the Adenosine triphosphate (ATP) viability test. As a result of the gene expression analysis, while 14 genes were not evaluated, expression profiles were obtained for 37 genes out of 51 genes. By the drug-protein interaction analyses, Topoisomerase I (TOPI), Topoisomerase 2 alpha (TOP2A), Topoisomerase 2 beta (TOP2B), Cyclin-dependent kinases 4 (CDK4), Cyclin-dependent kinases 6 (CDK6), ATP binding cassette subfamily B member 1 (ABCB1), ATP binding cassette subfamily C member 1 (ABCC1), ATP binding cassette subfamily C member 3 (ABCC3), B-cell leukemia/lymphoma 2 (BCL2), Poly (ADP-ribose) polymerase 1 (PARP1), Breast cancer gene 1 (BRCA1) and Cyclin dependent kinase inhibitor 1A (CDKN1A) genes and protein products were statistically significantly found to be in association with drug resistance. in bioinformatics analyses, it was observed that 13 pathways were affected due to expression changes and 12 genes related to these pathways were determined to activate multidrug resistance mechanisms. platinum-based drugs, as well as a broad range of other agents including topoisomerase and PARP1 inhibitors, and anthracyclines, have been shown to potentially possess multiple drug resistance. © 2024 bei den Autorinnen und Autoren, publiziert von Walter de Gruyter GmbH, Berlin/Boston 2024.
dc.identifier.citationDere, E., Akgün, O., Aztopal, N., & Ulukaya, E. (2025). Investigation into drug resistance to cisplatin in cancer stem cell-enriched population in non-small cell lung cancer. Turkish Journal of Biochemistry, (0).
dc.identifier.doi10.1515/tjb-2024-0181
dc.identifier.issn02504685
dc.identifier.scopus2-s2.0-85217040134
dc.identifier.scopusqualityQ3
dc.identifier.urihttp://dx.doi.org/10.1515/tjb-2024-0181
dc.identifier.urihttps://hdl.handle.net/20.500.12713/7230
dc.identifier.wosWOS:001407108600001
dc.identifier.wosqualityQ4
dc.indekslendigikaynakScopus
dc.indekslendigikaynakWeb of Science
dc.institutionauthorUlukaya, Engin
dc.institutionauthoridEngin Ulukaya / 0000-0003-4875-5472
dc.language.isoen
dc.publisherWalter de Gruyter GmbH
dc.relation.ispartofTurkish Journal of Biochemistry
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectCisplatin
dc.subjectDrug Resistance
dc.subjectLung Cancer
dc.subjectStem Cell
dc.titleInvestigation into drug resistance to cisplatin in cancer stem cell-enriched population in non-small cell lung cancer
dc.typeArticle

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