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  • 1
    Electronic Resource
    Electronic Resource
    Changes of G1 cyclins, cdk2, and cyclin A during the differentiation of HL60 cells induced by TPA (1994)
    Springer
    Molecular and cellular biochemistry 132 (1994), S. 31-37 
    Details
    ISSN: 1573-4919
    Keywords: cell cycle ; TPA ; cyclin ; cdk2 ; differentiation ; acute leukemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Differentiation induction by 12-o-tetradecanoyl 13-acetate (TPA) results in the growth arrest of HL60 cells in the G1 phase. However, little is known about the changes of cell cycle-regulating genes during this differentiation process. We investigated the changes of mRNA for various cyclins (A, C, D1, D2, D3 and E) and cdk2. Synchronized HL60 cells began to proliferate immediately after release from cell cycle block and cell cycle synchrony was obvious until the second S phase. TPA-treated cells accumulated in G1 phase within 24 h and most of the cells were arrested in this phase at 36 h. The expression of cyclins and cdk2 was studied by Northern blot hybridization or the reverse-transcription polymerase chain reaction (RT-PCR). TPA treatment altered the expression of all genes studied. The expression of cdk2 and cyclin A mRNA was markedly down-regulated. Cyclin E mRNA expression was also prominently down-regulated from 12 h to 36 h, at which time a second increase of its expression was observed in control cells. In contrast, the expression of cyclin D1 mRNA was induced by TPA, while its expression in control cells was undetectable by Northern blot hybridization throughout the cell cycle. Cyclin C expression was faint and fluctuated irrelevant of cell cycle, but its expression in both control and TPA-treated cells was higher than at baseline. Cyclin D2 expression remained stable in control cells and TPA treatment resulted in slight down-regulation at 12 h, but no difference was observed after 24 h. Cyclin D3 mRNA expression was slightly induced at 6 h, a time when its expression was down-regulated in control cells. At 48 h, these cyclins (C, D2, and D3) showed almost same level of expression as the control. These findings suggest that the down-regulation of cyclin A and cdk2 expression contributes to the G1 arrest of HL60 cells during monocytic differentiation induced by TPA and that cyclin D1 plays an additional role other than the regulation of cell cycle progression.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00925672
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  • 2
    Electronic Resource
    Electronic Resource
    Differing responses of G2-related genes during differentiation of HL60 cells induced by TPA or DMSO (1993)
    Springer
    Molecular and cellular biochemistry 119 (1993), S. 29-34 
    Details
    ISSN: 1573-4919
    Keywords: cell cycle ; differentiation ; G2 phase ; acute leukemia ; differentiation inducer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Differentiation leads to the cessation of cellular proliferation, but little is known about the molecular mechanisms of growth arrest. We compared the effect of two differentiation inducers, 12-o-tetradecanoyl 13-acetate (TPA) and dimethyl sulfoxide (DMSO) on both the cell-cycle and the modulation of G2-related genes in synchronized HL60 cells. TPA treatment of HL60 cells resulted in G1 arrest within 24 h. In contrast, the cell cycling of DMSO-treated cells was initially accelerated and they progressed to the second cycle before accumulating in the G1 phase. Expression of cyclin B, cdc25, wee1 and cdc2 was studied during cell cycle arrest by Northern blot hybridization. Expression of cyclin B, cdc25 and cdc2 fluctuated in association with cell cycle progression towards the G2/M phase, while wee1 expression remained constant in untreated cells. These four genes were highly expressed in TPA-treated cells for the first 12 h, but drastic down-regulation was seen at 18 h and expression became undetectable after 24 h. In contrast, no remarked changes of gene expression were seen in DMSO-treated cells. These findings suggest that cell cycle progression along with the initial process of differentiation in response to TPA differs from the response to DMSO and that the down-regulation of cdc2 expression by TPA-treated HL60 cells contributes to endorsement of G1 arrest.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00926850
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  • 3
    Electronic Resource
    Electronic Resource
    A macrolide antibiotic, roxithromycin, inhibits the growth of human myeloid leukemia HL60 cells by producing multinucleate cells (1995)
    Springer
    Molecular and cellular biochemistry 144 (1995), S. 191-195 
    Details
    ISSN: 1573-4919
    Keywords: roxithromycin ; macrolide antibiotics ; myeloid leukemia ; hyperploid ; multinucleate cell ; cytokinesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The antiproliferative effect of roxithromycin (RXM) was studied using human myeloid leukemia HL60 cells. RXM inhibited the growth of HL60 cells in a concentration-dependent manner, and significantly inhibited growth at concentrations above 75 μM. This growth inhibition was not associated with specific cell cycle arrest and DNA synthesis was not impaired. In addition, the number of viable cells remained almost unchanged in the presence of 100 νM RXM. RXM induced growth inhibition at least partly by the formation of multinucleate cells. Both flowcytometric and morphological examination revealed that more than 40% of the RXM-treated cells were binucleate. These findings demonstrate that RXM is a potent new modulator of cell cycle progression in HL60 cells and suggest that the inhibition of cytokinesis by this drug may provide a new model for studying mitosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00944399
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  • 4
    Electronic Resource
    Electronic Resource
    Differential responses to Bcl-2 family genes to etoposide in chronic myeloid leukemia K562 cells (2000)
    Springer
    Molecular and cellular biochemistry 206 (2000), S. 43-50 
    Details
    ISSN: 1573-4919
    Keywords: etoposide ; Bcl-XL ; Bax ; apoptosis ; K562 cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Etoposide is a potent anticancer agent that is used to treat various tumors. We have investigated the dose-dependent effect of etoposide on apoptosis using chronic myeloid leukemia K562 cells treated with low (5 μM) or high (100 μM) concentrations of the drug. At a low concentration, etoposide induced little apoptosis at 24 h, while about 20% of the cells showed apoptosis morphologically at a high concentration. Processing of caspase-3 was slightly detected from 12 h and became obvious at 24 h with 100 μM etoposide. Caspase-3-like protease activity was detected at 24 h with a high concentration. Moreover, these changes were accompanied by cleavage of poly ADP ribose polymerase (PARP). Changes of the mRNA levels of most apoptosis-regulating genes were not prominent at both concentrations, except for the rapid induction of c-IAP-2/HIAP-1 and the down-regulation of Bcl-XL by 100 μM etoposide. The downregulation of Bcl-XL protein occurred from 6 h, while Bax protein conversely showed a slight increase from 6 h. Taken together, the present findings show that the dose-dependent apoptotic effect of etoposide is based on a change in the balance between Bcl-XL and Bax, which precedes the activation of caspase-3.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007056727876
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  • 5
    Electronic Resource
    Electronic Resource
    Biological effects of a relatively low concentration of 1-b-D-arabinofuranosylcytosine in K562 cells: Alterations of the cell cycle, erythroid-differentiation, and apoptosis (1998)
    Springer
    Molecular and cellular biochemistry 187 (1998), S. 211-220 
    Details
    ISSN: 1573-4919
    Keywords: 1-β-D-arabinofuranosylcytosine ; cell cycle ; apoptosis ; differentiation ; K562 cells ; c-myc
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Therapeutic strategies for leukemia are directed to induction of differentiation and apoptosis as well as growth inhibition. One of the key antileukemic agents, 1-β-D-arabinofuranosylcytosine (ara C), is clinically applied according to these therapeutic aims. However, the molecular effects of 0.1 μg/ml of ara C, a concentration that corresponds to the serum level in leukemic patients on a conventional dose of ara C, have not been well disclosed. Here, we addressed these issues using K562 cells which derived from a blastic crisis of chronic myeloid leukemia. DNA synthesis of treated cells was suppressed from 1-6 h. But, it recovered at 12 h and no further inhibition was observed. The number of cells was not decreased but DNA fragmentation was observed at 72 h. The number of erythroid-differentiated cells also increased to 30% at 72 h. Along with treatment, no marked alteration of mRNAs for cell cycle-regulating genes was found and the retinoblastoma gene product remained hyperphosphorylated throughout treatment. The expression of mRNAs for apoptosis-regulating genes also remained unchanged, except for slight down-regulation of Bax. c-myc protein was not found later than 48 h, and Max mRNA was downregulated. c-jun was immediately induced, followed by the fluctuated expression level along with treatment. These findings suggest that the 0.1 μg/ml ara C changed the proliferation, differentiation and death of K562 cells in a biphasic manner. In the early phase, DNA synthesis was inhibited without altering the expression of cell cycle regulating-genes. In the latter phase, cell death and erythroid- differentiation occurred in accordance with the down-regulation of c-myc.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006874931249
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  • 6
    Electronic Resource
    Electronic Resource
    Changes of cell cycle-regulating genes in interferon-treated Daudi cells (1994)
    Springer
    Molecular and cellular biochemistry 136 (1994), S. 117-123 
    Details
    ISSN: 1573-4919
    Keywords: cell cycle ; interferon ; cyclin ; cyclin-dependent kinase ; cdc25 ; weel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Interferon (IFN) modulates the expression of several genes and some of themare considered to be responsible for the inhibition of cellular growth. However, the alterations of cell cycle-regulating genes produced by IFN still remain unclear. Accordingly, we studied the expression of cell cycle-regulating genes during IFN-induced growth arrest. Cell cycle synchronized and unsynchronized Daudi Burkitt lymphoma cells were treated with IFN. Both the cell cycle distribution and the expression of cell cycle-regulating genes (cdk2, cdc2, cyclins A, B, C, D3 cdc25, and well) were studied by flow cytometry and by Northern blot hybridization or the reverse-transcription polymerase chain reaction, respectively. Treated cells passed through the first G1 phase and gradually accumulated in the following G1 phase. Expression of cyclins A, B, and D3 oscillated along with the cell cycle progression in control cells, and the alterations of cyclin B expression were especially prominent. Both cdc2 and cdk2 also showed changes, but these were not so distinct as observed with cyclin B. Expression of cdc25 and weel was little affected by cell cycle progression. In IFN-treated cells, expression of cyclins A and B were down-regulated, while that of cyclin C was not. Cyclin D3 expression was also down-regulated at 48 h, followed by an increase at 72 h. Expression of both cdc2 and cdk2 was down-regulated, especially that of the later. Weel expression was down-regulated by IFN but, the expression of cdc25 remained stable. These findings suggest that the modulation of cell cycle-regulating genes, particular by cyclin A and cdk2, plays an important role in IFN-induced cellular growth arrest.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00926071
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  • 7
    Electronic Resource
    Electronic Resource
    Interferon modulates the messenger RNA of G1-controlling genes to suppress the G1-to-S transition in Daudi cells (1995)
    Springer
    Molecular and cellular biochemistry 152 (1995), S. 149-158 
    Details
    ISSN: 1573-4919
    Keywords: interferon ; cell cycle arrest ; cyclin-dependent kinase ; cyclin ; cyclin-dependent kinase activating kinase ; cyclindependent kinase inhibitor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Interferon (IFN) is one of the potent antiproliferative cytokines and is used to treat some selected cancers. IFN arrests the growth of Burkitt Iymphoma derived cell line Daudi cells in the G1 phase. G1-to-S progression is controlled by positive and negative regulatory genes. Therefore, we investigated the effects of IFN on G1-controlling genes. Expression of cyclin-dependent kinases (Cdks 2, 3, 4, 5, 6), MO 15/Cdk7, and cyclins E and H was studied to assess positive regulators, while p15Ink4B, p16Ink4, p18, p21CipI, and p27Kip1 were assessed as negative regulators. Cdks 2, 4, 6 and cyclin E were markedly down-regulated. MO15/Cdk7 expression showed little change, but its regulatory subunit (cyclin H) was down-regulated like cyclin E. Expression of p15Ink4B and p16Ink4 was not observed. p18 was induced until 48 h and its expression returned to the initial level at 72 h. In contrast, p21Cip1 mRNA expression remained at the baseline level throughout IFN treatment, while the expression of p27Kip1 increased at 48 and 72 h. Taken together, these data indicate that IFN changes the messenger RNA of G1-controlling genes towards the suppression of G1-to-S transition.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01076077
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