Characterization of imatinib-resistant K562 cell line displaying resistance mechanisms

Basit Öğe Kaydı
dc.authoridSüreyya Bozkurt / 0000-0002-1765-9894en_US
dc.authorscopusidSüreyya Bozkurt / 55540860700
dc.authorwosidSüreyya Bozkurt / AAP-1146-2020
dc.contributor.authorHekmatshoar, Yalda
dc.contributor.authorÖzkan, Tülin
dc.contributor.authorGüneş, Buket Altınok
dc.contributor.authorBozkurt, Süreyya
dc.contributor.authorKaradağ, Aynur
dc.contributor.authorKarabay, Arzu Zeynep
dc.contributor.authorSunguroğlu, Asuman
dc.date.accessioned2020-08-30T20:07:50Z
dc.date.available2020-08-30T20:07:50Z
dc.date.issued2018
dc.departmentİstinye Üniversitesi, Tıp Fakültesi, Temel Tıp Bilimleri Bölümüen_US
dc.description.abstractChronic myeloid leukemia (CML) is a hematopoietic malignancy characterized by the t(9; 22) and the related oncogene, BCR-ABL. Tyrosine kinase activity of fusion protein BCR-ABL is the main cause of CML. Even if imatinib is used as a tyrosine kinase inhibitor (TKI) for CML therapy. drug resistance may occur in patients and the clinical failure of imatinib treatment in resistant patients had resulted with the use of another alternative TKIs. BCR-ABL dependent and independent molecular mechanisms have crucial roles in drug resistance. To reveal the underlying molecular mechanisms which play significant roles in imatinib resistance in CML, we established K562 imatinib-resistant cell line (K562r5) which was continuously exposed to (5 mu M) imatinib to investigate molecular mechanisms which play significant roles in drug resistance. First of all, we analyzed T315I. M351T, F315L and F359C/L/V mutations with DNA sequencing as a BCR-ABL dependent mechanism in our cell lines. Moreover, we investigated BCR-ABL independent mechanisms such as apoptosis. autophagy, drug transport and DNA repair which affect drug resistance in these cell lines. In vitro cell viability was determined by MTT assay. DNA sequencing analysis was performed to detect BCR-ABL mutations. The apoptotic effect of imatinib on CML cell lines was tested by flow cytometric Annexin V-PE staining and caspase activation assays. Apoptotic, autophagic, drug transporter and DNA repair genes expression levels were determined by RT-PCR. The conventional cytogenetic analysis was performed on K562s and K562r cells. Our results indicate that inhibition of apoptosis, induction of autophagy, overexpression of efflux gene MDR1 and down-regulation of influx gene OCT1 play crucial roles in the progression of imatinib resistance.en_US
dc.identifier.citationHekmatshoar, Y., Ozkan, T., Gunes, B. A., Bozkurt, S., Karadag, A., Karabay, A. Z., & Sunguroglu, A. (2018). Characterization of imatinib-resistant K562 cell line displaying resistance mechanisms. Cellular and Molecular Biology, 64(6), 23-30.en_US
dc.identifier.doi10.14715/cmb/2018.64.6.5en_US
dc.identifier.endpage30en_US
dc.identifier.issn0145-5680en_US
dc.identifier.issn1165-158Xen_US
dc.identifier.issue6en_US
dc.identifier.pmid29808796en_US
dc.identifier.scopus2-s2.0-85047336465en_US
dc.identifier.scopusqualityQ4en_US
dc.identifier.startpage23en_US
dc.identifier.urihttps://doi.org/10.14715/cmb/2018.64.6.5
dc.identifier.urihttps://hdl.handle.net/20.500.12713/839
dc.identifier.volume64en_US
dc.identifier.wosWOS:000443102400004en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.institutionauthorBozkurt, Süreyyaen_US
dc.language.isoenen_US
dc.publisherC M B Assocen_US
dc.relation.ispartofCellular and Molecular Biologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectImatinib Resistanceen_US
dc.subjectCmlen_US
dc.subjectApoptosisen_US
dc.subjectAutophagyen_US
dc.subjectDrug Transporter Proteinsen_US
dc.subjectDna Repairen_US
dc.titleCharacterization of imatinib-resistant K562 cell line displaying resistance mechanismsen_US
dc.typeArticleen_US

Dosyalar

Orijinal paket
Listeleniyor 1 - 1 / 1
Küçük Resim Yok
İsim:
53.pdf
Boyut:
1.07 MB
Biçim:
Adobe Portable Document Format
Açıklama:
Tam Metin / Full Text
İndir

Koleksiyon

WoS İndeksli Yayınlar Koleksiyonu
PubMed İndeksli Yayınlar Koleksiyonu
Scopus İndeksli Yayınlar Koleksiyonu
Temel Tıp Bilimleri Bölümü Makale Koleksiyonu