Počet záznamů: 1
Exosomes released by imatinib-resistant K562 cells contain specific membrane markers, IFITM3, CD146 and CD36 and increase the survival of imatinib-sensitive cells in the presence of imatinib
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SYSNO ASEP 0544873 Druh ASEP J - Článek v odborném periodiku Zařazení RIV J - Článek v odborném periodiku Poddruh J Článek ve WOS Název Exosomes released by imatinib-resistant K562 cells contain specific membrane markers, IFITM3, CD146 and CD36 and increase the survival of imatinib-sensitive cells in the presence of imatinib Tvůrce(i) Hrdinová, T. (CZ)
Toman, O. (CZ)
Dresler, J. (CZ)
Klimentová, J. (CZ)
Šalovská, Barbora (UMG-J)
Pajer, P. (CZ)
Bartoš, O. (CZ)
Polívková, V. (CZ)
Linhartová, J. (CZ)
Poláková, K. (CZ)
Kabickova, H. (CZ)
Brodská, B. (CZ)
Krijt, M. (CZ)
Zivny, J. (CZ)
Vyoral, D. (CZ)
Petrák, J. (CZ)Celkový počet autorů 16 Zdroj.dok. International Journal of Oncology. - : Spandidos Publications - ISSN 1019-6439
Roč. 58, č. 2 (2021), s. 238-250Poč.str. 13 s. Forma vydání Online - E Jazyk dok. eng - angličtina Země vyd. GR - Řecko Klíč. slova chronic myeloid leukemia ; imatinib mesylate ; drug resistance ; proteomics ; exosome ; tyrosine kinase inhibitor ; surface marker Obor OECD Oncology CEP ED1.1.00/02.0109 GA MŠMT - Ministerstvo školství, mládeže a tělovýchovy Způsob publikování Omezený přístup Institucionální podpora UMG-J - RVO:68378050 UT WOS 000615889800001 DOI 10.3892/ijo.2020.5163 Anotace Chronic myeloid leukemia (CML) is a malignant hematopoietic disorder distinguished by the presence of a BCR-ABL1 fused oncogene with constitutive kinase activity. Targeted CML therapy by specific tyrosine kinase inhibitors (TKIs) leads to a marked improvement in the survival of the patients and their quality of life. However, the development of resistance to TKIs remains a critical issue for a subset of patients. The most common cause of resistance are numerous point mutations in the BCR-ABL1 gene, followed by less common mutations and multiple mutation-independent mechanisms. Recently, exosomes, which are extracellular vesicles excreted from normal and tumor cells, have been associated with drug resistance and cancer progression. The aim of the present study was to characterize the exosomes released by imatinib-resistant K562 (K562(IR)) cells. The K562(IR)-derived exosomes were internalized by imatinib-sensitive K562 cells, which thereby increased their survival in the presence of 2 mu M imatinib. The exosomal cargo was subsequently analyzed to identify resistance-associated markers using a deep label-free quantification proteomic analysis. There were >3,000 exosomal proteins identified of which, 35 were found to be differentially expressed. From this, a total of 3, namely the membrane proteins, interferon-induced transmembrane protein 3, CD146 and CD36, were markedly upregulated in the exosomes derived from the K562(IR) cells, and exhibited surface localization. The upregulation of these proteins was verified in the K562(IR) exosomes, and also in the K562(IR) cells. Using flow cytometric analysis, it was possible to further demonstrate the potential of CD146 as a cell surface marker associated with imatinib resistance in K562 cells. Taken together, these results suggested that exosomes and their respective candidate surface proteins could be potential diagnostic markers of TKI drug resistance in CML therapy. Pracoviště Ústav molekulární genetiky Kontakt Nikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217 Rok sběru 2022 Elektronická adresa https://www.spandidos-publications.com/10.3892/ijo.2020.5163
Počet záznamů: 1