Phenotypic and functional characterization of subpopulation of Imatinib resistant chronic myeloid leukemia cell line

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dc.contributor.authorHekmatshoar, Yalda
dc.contributor.authorKaradağ Gürel, Aynur
dc.contributor.authorÖzkan, Tülin
dc.contributor.authorSaadat, Yalda Rahbar
dc.contributor.authorKoç, Aslı
dc.contributor.authorKarabay, Arzu Zeynep
dc.contributor.authorBozkurt, Süreyya
dc.contributor.authorSunguroğlu, Asuman
dc.date.accessioned2023-07-17T07:27:01Z
dc.date.available2023-07-17T07:27:01Z
dc.date.issued2023en_US
dc.departmentFakülteler, Tıp Fakültesi, Temel Tıp Bilimleri, Tıbbi Biyoloji Ana Bilim Dalıen_US
dc.description.abstractPurpose: Chronic myeloid leukemia (CML) is a hematological malignancy characterized by the presence of BCR-ABL protein. Imatinib (IMA) is considered as the first line therapy in management of CML which particularly targets the BCR-ABL tyrosine kinase protein. However, emergence of resistance to IMA hinders its clinical efficiency. Hence, identifying novel targets for therapeutic approaches in CML treatment is of great importance. Here, we characterize a new subpopulation of highly adherent IMA-resistant CML cells that express stemness and adhesion markers compared to naive counterparts. Materials and methods: We performed several experimental assays including FISH, flow cytometry, and gene expression assays. Additionally, bioinformatics analysis was performed by normalized web-available microarray data (GSE120932) to revalidate and introduce probable biomarkers. Protein-protein interactions (PPI) network was analyzed by the STRING database employing Cytoscape v3.8.2. Results: Our findings demonstrated that constant exposure to 5 ​μM IMA led to development of the adherent phenotype (K562R-adh). FISH and BCR-ABL expression analysis indicated that K562R-adh cells were derived from the original cells (K562R). In order to determine the role of various genes involved in epithelial-mesenchymal transition (EMT) and stem cell characterization, up/down-regulation of various genes including cancer stem cell (CSC), adhesion and cell surface markers and integrins were observed which was similar to the findings of the GSE120932 dataset. Conclusion: Treating CML patients with tyrosine kinase inhibitors (TKIs) as well as targeting adhesion molecules deemed to be effective approaches in prevention of IMA resistance emergence which in turn may provide promising effects in the clinical management of CML patients.en_US
dc.identifier.citationHekmatshoar, Y., Karadağ Gürel, A., Özkan, T., Saadat, Y. R., Koç, A., Karabay, A. Z., Bozkurt, S., Sunguroğlu, A. (2023). Phenotypic and functional characterization of subpopulation of Imatinib resistant chronic myeloid leukemia cell line. Advances in medical sciences, 68(2), 238-248. 10.1016/j.advms.2023.06.002en_US
dc.identifier.endpage248en_US
dc.identifier.issn1896-1126
dc.identifier.issn1898-4002
dc.identifier.issue2en_US
dc.identifier.scopus2-s2.0-85164418056
dc.identifier.scopusqualityQ1
dc.identifier.startpage238en_US
dc.identifier.urihttps://hdl.handle.net/20.500.12939/3563
dc.identifier.volume68en_US
dc.identifier.wosWOS:001039154800001
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorHekmatshoar, Yalda
dc.language.isoen
dc.relation.ispartofAdvances in medical sciences
dc.relation.isversionof10.1016/j.advms.2023.06.002en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectChronic myeloid leukemiaen_US
dc.subjectDrug resistanceen_US
dc.subjectEpithelial–mesenchymal transitionen_US
dc.subjectPhenotype switchingen_US
dc.subjectTyrosine kinase inhibitorsen_US
dc.titlePhenotypic and functional characterization of subpopulation of Imatinib resistant chronic myeloid leukemia cell line
dc.typeArticle

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