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Expression of cyclin A, B1 and D1 after induction of cell cycle arrest in the Jurkat cell line exposed to doxorubicin

Authors

  • Agnieszka Żuryń,

    Corresponding author
    1. Department of Histology and Embryology, Nicolaus Copernicus University in Toruń, Collegium Medicum in Bydgoszcz, Karlowicza 24, 85-092 Bydgoszcz, Poland
      (email azuryn@cm.umk.pl)
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  • Anna Litwiniec,

    1. Plant Breeding and Acclimatization Institute-National Research Institute Radzików, Research Division in Bydgoszcz, Department of Genetics and Breeding of Root Crops, Laboratory of Biotechnology, Powstańców Wielkopolskich 10, 85-090 Bydgoszcz, Poland
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  • Lidia Gackowska,

    1. Department of Immunology, Nicolaus Copernicus University in Toruń, Collegium Medicum in Bydgoszcz, Sklodowskiej-Curie 9, 85-094 Bydgoszcz, Poland
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  • Andrzej Pawlik,

    1. Department of Histology and Embryology, Nicolaus Copernicus University in Toruń, Collegium Medicum in Bydgoszcz, Karlowicza 24, 85-092 Bydgoszcz, Poland
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  • Aleksandra Antonina Grzanka,

    1. Department of Dermatology and Sexually Transmitted Diseases, Nicolaus Copernicus University in Toruń, Collegium Medicum in Bydgoszcz, Kurpiskiego 5, 85-096 Bydgoszcz, Poland
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  • Alina Grzanka

    1. Department of Histology and Embryology, Nicolaus Copernicus University in Toruń, Collegium Medicum in Bydgoszcz, Karlowicza 24, 85-092 Bydgoszcz, Poland
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(email azuryn@cm.umk.pl)

Abstract

Jurkat human lymphoblastoid cells were incubated in increasing concentrations of doxorubicin (0.05, 0.1 and 0.15 μM) to induce cell death, and their expression of cyclin A, B1 and D1 was evaluated by flow cytometry (cell cycle progression, Annexin V assay, percentages and levels of each of the cyclins), transmission electron microscopy (ultrastructure) and confocal fluorescence microscopy (expression and intracellular localization of cyclins). After low-dose doxorubicin treatment, Jurkat cells responded mainly by G2/M arrest, which was related to increased cyclin B1, A and D1 levels, a low level of apoptosis and/or mitotic catastrophe. The influence of doxorubicin on levels and/or localization of selected cyclins was confirmed, which may in turn contribute to the G2/M arrest induced by the drug.

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