• Journal of Life Science
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• v.16 no.5
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• pp.759-766
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• 2006

Acute promyelocytic leukemia (APL) is a myeloid leukemia caused by over-expression of fusion protein, PML/RAR$({\alpha})$, which was the result of chromosomal translocation and induces the blockage of differentiation of affected promyelocytes. Pharmacological dose of retinoic acid induces the activation of and subsequent degradation of PML/RAR$({\alpha})$ fusion protein, and then APL cells undergo through the normal differentiation pathway. Arsenic trioxide has proved effective in causing remission of acute promyelocytic leukemia by inducing apoptosis of this tumor cells, whereas the heterogeneity of cellular susceptibility to this cytotoxic agent limited its usage on more types of tumors in clinic. This work showed that arsenic trioxide could induce apoptosis of a panel of acute promyelocytic leukemic cell lines, all-trans-retinoic acid (ATRA) sensitive NB4 cells and ATRA resistant UF-1 cell. They were investigated with regard to the correlation between the inherent or intrinsic cellular level of GSH and the apoptotic susceptibility of the cells to arsenic trioxide. We manifested, in two cell types, the inherently existed difference in intracellular GSH level reactive to the arsenic trioxide, and a positive correlation between the GSH level and their apoptotic sensitivity to arsenic trioxide. And it showed that arsenic trioxide could differentiate promyelocytic cancer cells to the cells possessed of dendritic cell surface markers. Unravelling the cause of the different susceptibility between leukemic cells and proving that promyelocyte could be differentiated to dendritic cells by arsenic trioxide will help not only to understand the mechanism underlying the complete remission of acute promyelocytic leukemia induced by arsenic trioxide, but also to expand its clinical usage.

• Korean Journal of Food Science and Technology
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• v.30 no.3
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• pp.665-671
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• 1998

Protein-bound polysaccharides (PBP) were extracted from the mycellia of Lentinus edodes SR-1, and their anti-tumor activities and immunopotentiating properties were observed. The amounts of PBP needed to extend the doubling time twofold (1 unit) were found to be 1 mg for mouse leukemic cells $P_{388}\;and\;L_{1210}$; 4.4, 3.6 and 6.6 for bowel cancer cells, HCT-48, HRT-18, HT-29 respectively; and 2.6 mg for liver cancer cell, Hep G2. When $P_{388}\;and\;L_{1210}$ were treated with 4 mg of PBP, more than 90% of the cell number were reduced in 48 hours. However, 9 mg of PBP and 72 hrs of incubation time were needed to obtain the same effect for HRT-18, HT-29, and Hep G2. The significant reduction of cell size was observed as the amount of PBP and the incubation time increased. Mice spleen weight and plaque forming cell number increased when the cancer cells were treated with PBP.

• Journal of Microbiology
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• v.34 no.4
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• pp.311-315
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• 1996

The retroviral Gag polyprotein directs the assembly of virion particles and plays an important role in some events after entry into a host cell. The Gag polyprotein of a virus mixture is responsible for inducing murine acquired immunodeficiency syndrome (MAIDS) when injected into susceptible strains of mice. In order to identify the host cellular proteins which interact with the MAIDS virus Gag proteins and possibly mediate the function of the Gag proteins, mouse T-cell leukemic cDNA expression library was screened using the yeast GAL4 two hybrid system. Of 11 individual positive clones, the clone Y1 was selected for the study of protein-protein interaction. Its DNA sequence revealed that it was an exact match to the murine SH3 domain-containing protein SH3P8. It is expressed as 2.4 kbp transcripts in testis at higher levels and in various tissues tested at lower levels. Glutathione S-transferase-Y1 fusion protein binds tightly to $Pr60^{def-gag}$ as well as $Pr65^{eco-gag}$.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1993.04a
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• pp.148-148
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• 1993

본 실험에서는 유전자 재조합으로 제조한 [$^{125}$ I]-labeled human GM-CSF을 사용하여 GM-CSF의 HL-60 (promyelocytic leukemic cell)의 표면에 존재하는 GM-CSF의 수용체의 특성을 알고 GM-CSF의 수용체에 어떤 parameter로 결합하는지를 밝히고 나아가 현재 사용되고 있는 유전자 재조합으로 제조된 Prokine(Sargramostim)과 Lucky에서 제조된 GM-CSF (LDB-005)의 수용체에 대한 결합율을 측정, 비교하고자 하였다. 본 실험의 결과를 보면 유전자 재조립으로 제조된 Human[$^{125}$ I] GM-CSF가 HL-60 cell에 대하여 선택적으로 결합하고 표면수용체에 saturable하게 결합함을 알 수 있었으며 scatchard analysis 결과한 종류의 GM-CSF의 K3값은 2.03$\times$$10^{9}$/M로($IC_{50}$/=~493pM) 세포당 결합부위의 수는 75개 정도로 J. DiPersio et al과 Linda S. Park et al.의 보고와 비슷한 결과를 얻었다.

• Korean Journal of Food Science and Technology
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• v.27 no.4
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• pp.445-448
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• 1995

This study was performed to observe cytotoxic effect of Acetobacter aceti OLS-001 extract against cancer cell lines, including mouse leukemic lymphocyte(P388, L1210) and human rectal(HRT-18) cell. The anticancer substance were prepared by ethanol precipitation of the glass bead extraction combined with hot water of Acetobacter aceti OLS-001. The growth rates of the cancer cells in medium containing Acetobacter aceti extract were inhibited gradually to a significant degree in proportion to the increase of the extract concentration. Morphology of HRT-18 cells in medium containing Acetobacter aceti extract were seen to be shrinked and fragmented.

• Archives of Pharmacal Research
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• v.25 no.4
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• pp.421-427
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• 2002

For probing the importance of planarity of imidazolidinone motif of 4-phenyl-1-(N-acylindoline-5-sulfonyl)imidazolidinones 1 for their cytotoxicity, 4-phenyl-1-(N-acylindoline-5-sulfonyl)[1,2,5]thiadiazolidine-1,1-dioxides 2 were prepared and their cytotoxicity were measured against human lung carcinoma (A549), human colon carcinoma (COLO205), human ovarian cancer (SK-OV-3), human leukemic cancer (K562), and murine colon adenocarcinoma (Colon26) cell lines in vitro. Although only carbonyl moiety of imidazolidinone ring was replaced with sulfonyl group, compounds 2 do not show any activity against all five cancer cell lines unlike 1. Therefore the planarity of imidazolidinone ring of 1 should be an important factor for their cytotoxic activity.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.148.1-148.1
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• 2003

Ceramide is an important lipid messenger involved in mediating a variety of cell functions including apoptosis. Previously, we have shown that ceramide induces Bax translocation which is associated with cytochrome c release from the mitochondria. In this study, we show that p38 MAP kinase is involved in ceramide-induced Bax translocation. In human leukemic cells, ceramide stimulated the phosphorylation of p38 MAP kinase. Preincubation of cells with SB203580, a specific inhibitor of p38 inhibited DNA fragmentation induced by cell-permeable ceramide. (omitted)

• Archives of Pharmacal Research
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• v.20 no.5
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• pp.410-413
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• 1997

In the course of screening synthetic compounds to inhibit tumor cell growth, pyrrolo[1,2-.alpha.] benzimidazole (PBI), an intermediate of azamitosene, was found to inhibit a proliferation of gastric cancer cell lines. Despite a potential cytotoxic activity against solid tumor cells as opposed to that against rapidly-doubled leukemic cells, there has been no report on the inhibition of gastric cancer cell line by PBI and its' derivatives. The present experiment was designed to determine if PBI derivatives can effectively inhibit the cellular proliferation of gastric cancer cells by using in vitro as well as in vivo chemosensitivity system (MTT assay, clonogenic assay and human tumor xenografted assay). Of the tested PBI derivatives, PBI (18) and PBI (20), displayed the effective growth inhibition of cultured gastric cancer cells or even in the xenografted nude mouse model.

• Korean Journal of Food Science and Technology
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• v.30 no.5
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• pp.1236-1242
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• 1998

Korean Lentinus edodes SR-1 was cultured to multiply the mycelia in the complete broth medium (C/N=13.1) for mushroom, and protein-bound polysaccharides were extracted from the cultured broth containing mycelia (The whole cultured broth was used to increase the yields: 80% of protein-bound polysaccharides were existed at the cell wall of mycelia and 20% of those were secreted extracellularily in this culture). Protein-bound polysaccharides in the cultured broth containing mycelia were extracted by using three different methods: 1) Extraction with hot water, 2) Disintegration of cell wall by glass bead mill treatment before extraction with hot water, and 3) Cellulase treatment before extraction with hot water. The highest yield was obtained (930 mg polysaccharides/100 mL culture broth) when protein-bound polysaccharides were extracted with 2) method. The extracted crude protein-bound polysaccharides were purified using protease, DEAE-cellulose and Sephadex G-100. The growth inhibition activity for $P_{388}$, mouse leukemic cell, increased (53.7, 62.2, 93.7% and 97.4%) as the purification level increased. Protein-bound polysaccharides contained 46.1% of polysaccharides, 7.3% of protein, and trace amounts of minerals. Polysaccharides contained glucose, galactose, xylose and mannose. The content of proline and glycine were high, however, methionine and leucine were not found. The major minerals were Na, K, Zn, and Ca.

• Journal of Marine Bioscience and Biotechnology
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• v.1 no.2
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• pp.76-83
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• 2006

Epidemiological studies have indicated that the ubiquitous consumption of seaweeds is a protective factor against some types of cancer. Previous results showed that the administration of seaweed powder or extract reduced the incidence rate of chemically induced tumorigenesis using in vivo animal model. Recently, we reported that the extracts of Gloiopeltis furcata, a kind of Korean edible seaweed, caused he cell growth inhibition of various human cancer cell lines, among them methanol extract exhibited a relatively strong antiproliferative activity. However, the molecular mechanisms of this seaweed in malignant cells have been poorly studied until now. To elucidate this problem, we investigated the effects of methanol extract of G. furcata (MEGF) on the growth inhibition in several human cancer cell lines, and further we analyzed the effects of this extract were tested on the activity of apoptosis induction in human leukemic cells. The results demonstrated that MEGF treatment resulted in the morphological changes and the growth inhibition in a dose-dependent manner. Furthermore, MEGF potently suppresses the growth of human leukemic U937 cells by induction of apoptosis, which was associated with induction of cyclin-dependent kinase inhibitor p21(WAF1/CIP1) in a tumor suppressor p53-independent fashion and up-regulation of Fas/FasL system. Further studies will be needed to identify the active compounds that confer the anticancer activity of MEGF. Once such compounds are identified, the mechanisms by which they exert their effects can begin to be characterized.