• The Journal of the Korea Contents Association
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• v.14 no.6
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• pp.241-246
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• 2014

Acute promyelocytic leukemia (APL) is a cancer of the blood. Although electron beam (EB) irradiation is used with other anti-cancer agents, EB irradiation can be harmful to normal tissues around the cancer. In the present study, we evaluate the differential cytotoxic effect of EB irradiation with other molecules, including TNF-${\alpha}$, on DMSO-treated HL-60 cells and HL-60 cells. HL-60 cells are the human promyleocytic leukemia cell line and are differentiated by DMSO. DMSO-treated HL-60 cells are considered to be normal granulocytic cells. In these results, TNF-${\alpha}$ may be used as the potential agent for the treatment of blood cancer without side effects in low dose of EB irradiation therapy.

• Korean Journal of Microbiology
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• v.51 no.2
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• pp.115-125
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• 2015

A monoclonal antibody AP64 IgM binds to human acute nonlymphocytic leukemia (ANLL) cell line HL60 and also cross-reacts with the homologous antigen in a rat ANLL cell. This antibody mediated by complement, has leukemia a suppression effect. In this study, we generated a recombinant single-chain variable domain fragment (ScFv) which were derived from $V_H$ and $V_L$ cDNA of AP64 IgM-secreting hybridoma by RT-PCR. The two variable regions were joined with a single 15 amino acid linker $(G_4S)_3$. This recombinant ScFv was expressed as a single polypeptide chain from Escherichia coli BMH 71-18. The recombinant ScFv was purified by applying the periplasmic extract to $Ni^+$-NTA-agarose affinity column and detected with westernblot. The purified recombinant ScFv recognized a surface antigen (about 30 kDa) of HL60 cell line which is the same antigen detected by parental AP64 IgM. But the affinity of ScFv for a surface antigen of HL60 was lower than that of the parental AP64 IgM, which needs to be further improved. Overall, the recombinant ScFv specific to HL60 might be a useful bioreagent for either diagnostic or therapeutic purposes.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.159.2-159.2
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• 2003

Codonopside lc is an active natural compound isolated from the roots of Codonopsis lanceolata (Campanulaceae), a Korean medicinal herb. In the present study, we investigated the in vitro effect of Codonopside 1c on the proliferation and induction of apoptosis in HL-60 human promyelocytic cells. When HL-60 cells were treated with Codonopside 1c, evidence of apoptotic features, including DNA fragmentation, formation of DNA ladder in agarose gel elecrophoresis and increse of annexin V binding, were obtained. (omitted)

• Proceedings of the PSK Conference
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• 2002.04a
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• pp.158.1-158.1
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• 2002

• Biomedical Science Letters
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• v.19 no.2
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• pp.118-123
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• 2013

Tumor necrosis factor-alpha (TNF-${\alpha}$) is a proinflammatory cytokine that mediates the inflammatory response and immune functions, and modulates the proliferation, differentiation and cell death of cancer cells. The differential functions of TNF-${\alpha}$ in various human cells due to the formation of different stimulating pathway upon the binding of TNF-${\alpha}$ to its receptors. In the present study, we examined the different effects of TNF-${\alpha}$ on the survival and apoptosis between normal granulocytes and human myeloid leukemia HL-60 cells. Although TNF-${\alpha}$ did not affect on the constitutive apoptosis of granulocytes, TNF-${\alpha}$ strongly induced the apoptosis of HL-60 cells in a dose- and a time-dependent manner. TNF-${\alpha}$-induced apoptosis was occurred via the activation of caspase 8, caspase 9 and caspase 3/7 and the induction of ROS production in HL-60 cells. Also, BAY-11-7085, a NF-${\kappa}B$ inhibitor, blocked the TNF-${\alpha}$-induced apoptosis in HL-60 cells. NF-${\kappa}B$ may be involved in TNF-${\alpha}$-induced apoptotic signaling pathway in HL-60 cells. These results suggest that TNF-${\alpha}$ activates apoptotic pathways and its process depends on cell type and many cellular factors. A better understanding of the differential effect of TNF-${\alpha}$ on cell apoptosis and survival may provide important information that can be used to elucidate the specific inhibitory effect of TNF-${\alpha}$ on the cancer dis.

• The Korean Journal of Mycology
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• v.27 no.4 s.91
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• pp.312-317
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• 1999

In order to study the antitumoral effect of meju extracts, which was made with a single inoculum of the microorganism, the cytotoxicity effects on several human leukemia cells such as promyelocytic leukemia cell (HL60), histiocytic lymphoma cell (U937) and acute T-cell leukemia Jurkat cell, and lymphocyte were analyzed by MTT assay. Twenty one microbes, mainly fungal genera, were isolated from Korean traditional mejus of different regions. From those collected isolates, meju was manufactured and extracted with 80% methanol, respectively. Meju methanol extracts exhibited low activites in cytotoxicity tests on HL60 cell, but high antitumoral effects of meju methanol extracts were shown on U937 and Jurkat cells. Meju methanol extracts made with a genera of Mucor, Absidia and Aspergillus showed prominant cytotoxic activities, especially. However all these extracts had no inhibitory effects on the cell growth of lymphocyte under the same conditions.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.1
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• pp.79-86
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• 2001

Recent clinical studies have shown that a high proportion of patients with acute promyelocytic leukemia (APL) achieve complete remission after treatment with all-trans retinoic acid (ATRA). However, most patients who receive continuous treatment with ATRA relapse and develop ATRA-resistant leukemia. Dendritic cells (DCs) are important antigen-presenting cells in the development of antileukemic T-cell responses. In this study, we investigated the strategies to overcome ATRA resistance of APL cells by inducing the differentiation of DCs from human leukemic cell lines for the developtment of adoptive immunotherapy. CD83 was used as a mature DC marker in this study and the expression of CD83 mRNA was determined by RT-PCR method. The promyelocytic leukemic cell line HL-60, B lymphoblast cell lines RPMI 7666 and NC-37 could be induced to dendritic cells in vitro. Treatment of HL-60 with phorbol 12-myristate 13-acetate (PMA) resulted in the expression of myeloid-related DC phenotypes, while treatment of RPMI 7666 with fms-like tyrosine kinase 3 ligand (Flt3-ligand, FL) and treatment of NC-37 with PMA and FL led to the expression of lymphoid-related DC phenotypes. In conclusion, myeloid-related DC phenotypes and lymphoid-related DC phenotypes could be generated from HL-60, NC-37 and RPMI 7666 cell lines, respectively. These DC phenotypes can potentially be used to generate antileukemic T cells in vitro for adoptive immunotherapy.

• Archives of Pharmacal Research
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• v.18 no.6
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• pp.396-401
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• 1995

As a part of trials to develop the antitumor agent from tannins isolated from plants, the antitumor activity of peduculagin, an ellagitannin, isolated from Alnus hirsuta var. microphylla was examined in vitro and in vivo. In vitro, the cytotoxicity was determined by 0.4% typanblue dye exclusion method. peduculagin showed the dose-dependent cytotoxicity against human chronic myelogenous leukemia (K-562), human promyelocytic leukemia (HL-60), mouse lymphoid neoplasm (P388), mouse lymphocytic leukemia (L1210) and mouse sarcoma 180(S180) cell lines. $ED_{50}\; values\; (ED_{50})$ of each cell line were 5.30, 0.92, 2.78, 9.35 and $1.38 \mug/ml$ respectively. The most sensitive cell line was HL-60. In vivo, pedunculagin was administered to ICR mouse with the doses of 50 and $100{\;}{\mu}g/ml$intraperitoneally once at 20 days before S180 inoculation. peduculagin showed the antitumor activity and its T/C ratio (%) was 120.82% in the group of both concentrations.

• Korean Journal of Veterinary Research
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• v.59 no.4
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• pp.195-199
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• 2019

Disulfiram (DSF) is a member of the dithiocarbamate family that can bind copper. Recent studies have shown that DSF has anti-cancer activities, but the mechanism has not been clarified. Therefore, it is important to study the action mechanism of DSF to maximize its anticancer effects. A human leukemia cell line, HL-60, was used in this study. HL-60 cells were treated with DSF and the cellular metabolic activity was measured. DSF increased the cell death of HL-60 cells in annexin V-fluorescein isothiocyanate/propidium iodide staining analysis. In addition, DSF decreased the mitochondrial membrane potential (MMP) of the HL-60 cells. The cytotoxicity of DSF on HL-60 cells was observed at 0.4 μM. Interestingly, the reduction of MMP by DSF was recovered by N-acetyl-L-cysteine, an inhibitor of reactive oxygen species (ROS) production. This suggests that the decrease in MMP by DSF is closely related to the production of ROS in HL-60 cells, which indicates the relationship between the apoptosis of HL-60 cells by DSF and the role of the mitochondria. This study provides clinicians and researchers with valuable information regarding the anti-cancer activity of DSF in terms of the action mechanism.

• Journal of Microbiology and Biotechnology
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• v.13 no.4
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• pp.607-612
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• 2003

To elucidate the action mechanism of MCS-C2, a novel analogue of toyocamycin and sangivamycin, its effect on the expression of cell cycle-related proteins in the human myelocytic leukemia cell line HL-60 was examined using Western blotting and a flow cytometric analysis. MCS-C2, a selective inhibitor of cyclin-dependent kinases, was found to inhibit cell growth in a time- and dose-dependent manner, and inhibits cell cycle progression by inducing the arrest at G1 and G2/M phases, in HL-60 cells. The flow cytometric analysis revealed an appreciable arrest of cells in the G2/M phase of the cell cycle after treatment with MCS-C2. The HL-60 cell population increased gradually from 13% at 0 h, to 28% at 12 h in the G2/M phase, after exposure to $2{\;}\mu\textrm{M}$ MCS-C2. Furthermore, Western blot analysis demonstrated that MCS-C2 induced the cell cycle arrest at G1 phase through the inhibition of pRb phosphorylation. Hypophosphorylated pRb accumulated after treatment with $5{\;}\mu\textrm{M}$ MCS-C2 for 12 h, whereas, the level of hyperphosphorylated pRb was reduced. Thus, treatment of the cell with MCS-C2 suppressed the hyperphosphorylated form of pRb with a commensurate increase in the hypophosphorylated form.