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1

Promoted megakaryocytic differentiation of K562 cells through oxidative stress caused by near ultraviolet irradiation

100%
Nurhayati R. W., Ojima Y., Nomura N., Taya M.
Cellular and Molecular Biology Letters
|
2014
|
tom 19
|
nr 4
Reactive oxygen species (ROS) have been proven to be important activators for various cellular activities, including cell differentiation. Several reports showed the necessity of ROS during cell differentiation of the megakaryocytic (MK) lineage. In this study, we employed near ultraviolet (near-UV) irradiation to generate endogenous oxidative stress in an MK differentiation process of K562 cells with phorbol 12-myristate 13-acetate (PMA) induction. A significant increase in the intracellular ROS level was detected on day 1 after near-UV irradiation. In the initial stage of differentiation, a shifted fraction of G1 and G2 phase cells was obtained using near-UV irradiation, giving an increased percentage of G2 phase cells (up from 31.1 to 68.7%). The near-UV irradiation-induced upregulation of the p21 gene, which is a cell cycle inhibitor, suggested that the G2 phase cells were prevented from undergoing cell division. It was found that the percentage of high ploidy (8N and 16N) cells was enhanced significantly at the later stage of the K562 cell culture with near-UV irradiation. Moreover, time-lapse analysis showed that near-UV irradiation encouraged the expression of CD41, a specific surface marker of megakaryocytes. This is the first report that the elevated oxidative stress through the near-UV irradiation promoted the MK differentiation of PMA-induced K562 cells.
2

Combined effects of doxorubicin and STI571 on growth, differentiation and apoptosis of CML cell line K562

84%
Jakubowska J., Stasiak M., Szulawska A., Bednarek A., Czyz M.
Acta Biochimica Polonica
|
2007
|
tom 54
|
nr 4
839-846
STI571 (imatinib mesylate; Gleevec®) is an inhibitor that targets the tyrosine kinase activity of Bcr-Abl present in chronic myelogenous leukemia (CML) cells. Some preclinical studies have demonstrated that the combination of STI571 with chemotherapeutic drugs results in enhanced toxicity in Bcr-Abl-positive leukemias. We investigated the potential benefit of using STI571 to down-regulate Bcr-Abl activity for the enhancement of doxorubicin anti-proliferative action in K562 cell line derived from blast crisis of CML. At low concentrations of both drugs (40 nM doxorubicin combined with STI571 in the range of 100–150 nM), the antiproliferative effects were mainly due to cellular differentiation as assessed by benzidine staining for hemoglobin synthesis level and real-time PCR for γ-globin expression. Higher concentrations of STI571 used in combinations with doxorubicin caused mainly apoptosis as shown by DNA degradation and nuclear fragmentation visualized by fluorescence microscopy after DAPI staining, changes in cell morphology observed after Giemza-May Grünwald staining and cellular membrane organization estimated by flow cytometry after Annexin V staining. As compared with either drug alone, cotreatment with STI571 and DOX induced stronger cellular responses. A low concentration of STI571 in combination with a low concentration of DOX might be tested as an alternative approach to increasing the efficacy of chemotherapy against CML
3

Monitoring of membrane phospholipid scrambling in human erythrocytes and K562 cells with FM1-43 - a comparison with annexin V-FITC

84%
Wrobel A., Bobrowska-Hagerstrand M., Lindqvist C., Hagerstrand H.
Cellular and Molecular Biology Letters
|
2014
|
tom 19
|
nr 2
The styryl dye FM1-43 becomes highly fluorescent upon binding to cell membranes. The breakdown of membrane phospholipid asymmetry in ionophore-stimulated T-lymphocytes further increases this fluorescence [Zweifach, 2000]. In this study, the capacity of FM1-43 to monitor membrane phospholipid scrambling was explored using flow cytometry in human erythrocytes and human erythrocyte progenitor K562 cells. The Ca2+-dependent phosphatidylserine-specific probe annexin V-FITC was used for comparison. The presented data show that the loss of phospholipid asymmetry that could be induced in human erythrocytes by elevated intracellular Ca2+ or by structurally different membrane intercalated amphiphilic compounds increases the FM1-43 fluorescence two- to fivefold. The profile of FM1-43 fluorescence for various treatments resembles that of phosphatidylserine exposure reported by annexin V-FITC. FM1-43 detected the onset of scrambling more efficiently than annexin V-FITC. The amphiphile-induced scrambling was shown to be a Ca2+-independent process. Monitoring of scrambling in K562 cells caused by NEM-induced Ca2+-release from intracellular stores and by Ca2+ and ionophore A23187 treatment showed that the increase in FM1-43 fluorescence correlated well with the number of annexin V-FITC-detected phosphatidylserine-positive cells. The results presented here show the usefulness of FM1-43 as a Ca2+-independent marker of dissipation in asymmetric membrane phospholipid distribution induced by various stimuli in both nucleated and non-nucleated cells.
4

Hyperthermia can differentially modulate the repair of doxorubicin-damaged DNA in normal and cancer cells

84%
Blasiak J., Widera K., Pertynski T.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr 1
Hyperthermia can modulate the action of many anticancer drugs, and DNA repair processes are temperature-dependent, but the character of this dependence in cancer and normal cells is largely unknown. This subject seems to be worth studying, because hyperthermia can assist cancer therapy. A 1-h incubation at 37°C of normal human pe­ripheral blood lymphocytes and human myelogenous leukemia cell line K562 with 0.5 juM doxorubicin gave significant level of DNA damage as assessed by the alkaline comet assay. The cells were then incubated in doxorubicin-free repair medium at 37°C or 41°C. The lymphocytes incubated at 37°C needed about 60 min to remove com­pletely the damage to their DNA, whereas at 41°C the time required for complete re­pair was shortened to 30 min. There was also a difference between the repair kinetics at 37°C and 41°C in cancer cells. Moreover, the kinetics were different in doxorubicin-sensitive and resistant cells. Therefore, hyperthermia may significantly affect the kinetics of DNA repair in drug-treated cells, but the magnitude of the effect may be different in normal and cancer cells. These features may be exploited in cancer chemotherapy to increase the effectiveness of the treatment and reduce unwanted ef­fects of anticancer drugs in normal cells and fight DNA repair-based drug resistance of cancer cells.
5

GATA-1 binding to the alphaV promoter negatively regulates expression of the integrin alphaV subunit in human leukemic K562 cells

84%
Czyz M., Stasiak M., Boncela J., Cierniewski C. S.
Acta Biochimica Polonica
|
2002
|
tom 49
|
nr 1
Recently we observed that the transcription factors Sp1 and Sp3 bind to the CTCCTCCTC sequence located between positions -194 and -172 of the αv promoter region and are directly involved in the regulation of transcriptional activity of the αv gene in human umbilical vascular endothelial cells (HUVECs) (Czyz & Cierniewski, 1999, Eur. J. Biochem. 265, 638). In this report we provide evidence that the GATA-1 factor regulates αv expression during differentiation of pluripotent K562 cells in­duced either by phorbol 12-myristate 13-acetate (PMA) or butyric acid (BA) through interaction with the GATA element in the «v gene promoter. DNase I footprinting analysis revealed that region -413 to -408, covering the GATA binding site, was pro­tected by nuclear extract from K562 cells. There was no protection of this region by HUVEC nuclear extract. Electrophoretic mobility shift assay (EMSA) analysis of nu­clear extract of K562 cells treated with BA revealed an increase in GATA binding ac­tivity, which was associated with reduced αv mRNA and αv protein on the cell surface. Stimulation of K562 cells with PMA resulted in opposite effects: lower expression of GATA-1 was associated with increased levels of αv. We conclude that the GATA-1 tran­scription factor specifically binds to the GATA element in the αv gene promoter and negatively regulates αv gene expression.
6

Effect of arsenic trioxide (Trisenox) on actin organization in K-562 erythroleukemia cells

67%
Izdebska M., Grzanka A., Ostrowski M., Zuryn A., Grzanka D.
Folia Histochemica et Cytobiologica
|
2009
|
tom 47
|
nr 3
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