Targeting Integrin α2 to Overcome Imatinib Resistance in Chronic Myeloid Leukemia Cells

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dc.contributor.authorHekmatshoar, Yalda
dc.contributor.authorÖzkan, Tülin
dc.contributor.authorKarabay, Arzu Zeynep
dc.contributor.authorBozkurt, Süreyya
dc.contributor.authorKaradağ Gürel, Aynur
dc.contributor.authorKurnaz Gömleksiz, Özlem
dc.contributor.authorFışgın, Tunç
dc.contributor.authorSunguroğlu, Asuman
dc.date.accessioned2025-10-16T06:58:40Z
dc.date.available2025-10-16T06:58:40Z
dc.date.issued2025
dc.departmentFakülteler, Tıp Fakültesi, Temel Tıp Bilimleri, Tıbbi Biyoloji Ana Bilim Dalı
dc.description.abstractChronic myeloid leukemia (CML) is a blood disorder caused by a genetic alteration that creates the BCR-ABL fusion gene, leading to continuous activation of cell growth signals and uncontrolled proliferation of the blood cells. Imatinib (IMA) resistance remains a major obstacle in CML treatment. Integrins, particularly integrin α2 (ITGA2), have been associated with cancer progression and drug resistance. In the current study, we investigated the role of ITGA2 in IMA resistance using IMA-sensitive K562 (K562S) and IMA-resistant K562 (K562R) cells. Our findings showed that ITGA2 is overexpressed in K562R cells and ITGA2 inhibitor E7820 (2.5 µM) treatment significantly decreased cell viability and induced apoptosis in both sensitive and resistant cells. Combination treatment with E7820 and imatinib enhanced pro-apoptotic gene expression (BAX, BIM) and decreased anti-apoptotic BCL2 levels in imatinib-resistant K562R cells. Flow cytometry confirmed ITGA2 inhibition at the protein level, and rhodamine assays revealed reduced MDR1 activity in treated cells. These results demonstrate that targeting ITGA2 may overcome imatinib resistance and offer a novel therapeutic strategy for CML.
dc.identifier.citationHekmatshoar, Y., Ozkan, T., Karabay, A. Z., Bozkurt, S., Gurel, A. K., Gomleksiz, O. K., ... & Sunguroglu, A. (2025). Targeting Integrin α2 to Overcome Imatinib Resistance in Chronic Myeloid Leukemia Cells. Biomolecules, 15(9), 1245. 10.3390/biom15091245
dc.identifier.doi10.3390/biom15091245
dc.identifier.issn2218-273X
dc.identifier.issue9
dc.identifier.pmid41008552
dc.identifier.scopus2-s2.0-105017408431
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://hdl.handle.net/20.500.12939/5962
dc.identifier.volume15
dc.identifier.wosWOS:001580368900001
dc.identifier.wosqualityQ1
dc.indekslendigikaynakPubMed
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.institutionauthorHekmatshoar, Yalda
dc.institutionauthorFışgın, Tunç
dc.language.isoen
dc.publisherBasel
dc.relation.ispartofBiomolecules
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectE7820
dc.subjectapoptosis
dc.subjectchronic myeloid leukemia
dc.subjectimatinib resistance
dc.subjectintegrin α2
dc.titleTargeting Integrin α2 to Overcome Imatinib Resistance in Chronic Myeloid Leukemia Cells
dc.typeArticle

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