• Environmental Mutagens and Carcinogens
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• v.22 no.1
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• pp.54-59
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• 2002

We have used cDNA microarray hybridization to identify gene regulated in response to gamma-irradiation in U-937 cell. The cDNA-chip was composed entirely of 1,000 human cancer related gene including apoptosis and angiogenesis etc. In gamma-irradiated U-937 cell, highly charged protein, ribosomal protein L32, four and a half LIM domains 3, lipocalin 2 (oncogene 24p3) and interleukin 15, ataxia telangiectasia mutated (includes complementation groups A, C and D) genes showed increased level of its transcription, and cell division cycle 25A, dihydrofolate reductase, topoisomerase (DNA) II beta(180kD), kinase suppressor of ras and strarigin genes showed reduced level of its transcription compared to untreated U-937 cell. The significant change of level of transcription was not found in well-known ionizing radiation(IR)-responsive gene, such as transcription factor TP53 and p53 related gene, except ataxia telangiectasia mutated gene.

• Journal of Ginseng Research
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• v.33 no.4
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• pp.324-329
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• 2009

Cell-cell adhesion managed by various adhesion molecules is known to be one of pathophysiological phenomena found in numerous immunological diseases such as rheumatoid arthritis and allergic diseases. In this study, we examined the regulatory role of ginsenosides (G)- Rh1, reported to display anti-inflammatory and anti-allergic effects, on CD29-mediated cell adhesion. G-Rh1 significantly suppressed U937 cell-cell adhesion mediated by CD29 but not CD43. It also blocked U937 cell-fibronectin adhesion, mediated by activated CD29, up to 30%. In agreement, this compound also significantly decreased the surface level of CD29 but not CD43 as well as other costimulatory molecules such as CD69, CD80, and CD86. Therefore, these results suggest that G-Rh1 may have inhibitory function on CD29-mediated cell adhesion events, probably contributing to its anti-inflammatory and anti-allergic activities.

• Journal of Life Science
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• v.17 no.4 s.84
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• pp.552-560
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• 2007

Histone deacetylase (HDAC) is overexpressed in a variety of cancers and is closely correlated with oncogenic factors. HDAC inhibitors such as trichostatin A(TSA) and sodium butyrate (Na-B) have been shown to induce apoptosis in vitro and in vivo in many cancer cells. The anti-apoptotic Bcl-2 protein has the remarkable ability to prevent cell death and Bcl-2 overexpression has been reported to protect against cell death. We previously reported that the apoptotic cell death of human leukemic U937 cells by TSA and Na-B treatment was associated with the down-regulation of Bcl-2 expression and activation of caspases. In the present study, we investigated the effects of Bcl-2 overexpression on the growth inhibition, cell cycle arrest and apoptosis induced by TSA and Na-B in U937 cells. TSA-induced growth inhibition, cell cycle arrest and apoptosis were significantly attenuated in Bcl-2 overexpressing U937/Bcl-2 cells however Na-B did not affected. Induction of apoptosis by TSA was accompanied by down-regulation of Bcl-2 expression, activation of caspase-3, -8 and -9, and degradation of DNA fragmentation factor/inhibitor of caspase-activated DNase, which was blocked by the overexpression of Bcl-2. Collectively, these findings suggest that ectopic expression of Bcl-2 appeared to inhibit TSA-induced apoptosis by interfering with inhibition of Bcl-2 and caspase activation.

• YAKHAK HOEJI
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• v.53 no.3
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• pp.119-124
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• 2009

Cell-cell adhesion managed by various adhesion molecules plays an important role in regulating functional activation of cells. This event mediates attachment of inflammatory cells to endothelial cells, interaction of antigen-presenting cells with T cells and metastatic adherence of cancer cells to epithelial tissue cells. Therefore, this cellular response is considered as one of therapeutic target to treat various cancers and inflammatory diseases. To develop proper model for evaluation of functional activation of adhesion molecules, the ability of U937 and Jurkat T cells responsive to various adhesion inducers such as phorbal-12-myristate-13-acetate (PMA), staurosporin and monoclonal antibodies to CD29, CD43 and CD98 was investigated using quantitative cell-cell adhesion assay. U937 cells made more cell-cell clusters by the treatment of antibodies to CD29 and CD43 than Jurkat T cells, while Jurkat T cells exhibited increased cell-cell adhesion ability in CD98 antibody treatment. In agreement, the surface levels of CD29 and CD98 were highly observed in U937 and Jurkat T cells, respectively. Therefore, our data suggest that Jurkat T and U937 cells can be used for model system to evaluate functional activation of adhesion molecules such as CD29 and CD98.

• YAKHAK HOEJI
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• v.39 no.5
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• pp.541-547
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• 1995

In order to investigate the usability of PALMIWON as antidiabetic immuno-modulating prescription for Insulin-dependent diabetes, we studies the effects of PALMIWON on immune cell and ${\beta}-cell$. U937 was used as the model of immune cell and RINm5F as the model of ${\beta}-cell$. The effects of PALMIWON was measured by cell viability in terms of MIT assay. As a result, PALMIWON and the compositional drugs showed the different effects m immune cell and ${\beta}-cell$. Cell viability of U937 was significantly decreased wheras that of RINm5F was no significantly difference between drug treated group and control, or significantly less reduction compared with U937. It implies that PALMIWON is useful as immunotherapeutic agents in the prevention and therapy of type 1 diabetes.

• Journal of Physiology & Pathology in Korean Medicine
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• v.25 no.1
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• pp.29-36
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• 2011

Nardostachyts chinensis (N. chinensis) belonging to the family Valerianaceae has been used to elicit stomachic and sedative effects. The MAPKs are serine/threonine kinases involved in the regulation of various cellular responses, such as cell proliferation, differentiation and apoptosis. The PKC also plays a key role in regulating the response of hematopoietic cells to both physiological and pathological inducers of proliferation and differentiation. This study investigated the signaling pathways on the U937 cell differentiation induced by N. chinensis. N. chinensis induced the differentiation of U937 cells, as shown by increased of differentiation surface antigen CD11b. Activation of ERK increased time-dependently in differentiation of U937 cells induced by N. chinensis, but activations of JNK and p38 were unaffected. Inhibitor of ERK (PD98059) significantly reduced CD11b expression induced by N. chinensis in U937 cells. In addition, N. chinensis increased protein level of PKC ${\beta}$I and PKC ${\beta}$II isoforms, but the protein level of PKC ${\alpha}$ and PKC ${\gamma}$was constant. PKC inhibitors (GF 109203X and H-7) inhibited U937 cell differentiation and the ERK activation induced by N. chinensis. These results indicated that PKC and ERK may be involved in U937 cell differentiation induced by N. chinensis.

• Journal of Life Science
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• v.16 no.4
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• pp.589-597
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• 2006

Genistein, a natural isoflavonoid phytoestrogen, is a strong inhibitor of protein tyrosine kinase and DNA topoisomerase activities. There are several studies documenting molecular alterations leading to cell cycle arrest and induction of apoptosis by genistein as a chemopreventive agent in a variety of cancer cell lines; however, its mechanism of action and its molecular targets on human bladder carcinoma and leukemic cells remain unclear. In the present study, we have addressed the mechanism of action by which genistein suppressed the proliferation of T24 bladder carcinoma and U937 leukemic cells. Genistein significantly inhibited the cell growth and induced morphological changes, and induced the G2/M arrest of the cell cycle in both T24 and U937 cells with a relatively stronger cytotoxicity in U937. The G2/M arrest in T24 cells was associated with the inhibition of cyclin A, cyclin B1 and Cdc25C protein expression without alteration of tumor suppressor p53 and cyclin-dependent kinase (Cdk) inhibitor p21(WAF1/CIP1). However, the inhibitory effects of genistein on the cell growth of U937 cells were connected with a marked inhibition of cyclin B1 and an induction of Cdk inhibitor p21 proteins by p53-independent manner. These data suggest that genistein may exert a strong anticancer effect and additional studies will be needed to evaluate the different mechanisms between T24 and U937 cells.

• Journal of Life Science
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• v.19 no.5
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• pp.620-624
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• 2009

D-Ala2-Leu5-enkephalin (DADLE), a hibernation inducer, can induce hibernation-like state in vivo and in vitro. We treated U937 human leukemia cancer cells with DADLE and investigated its possible effect on transcription and proliferation. Treatment of U937 cells with DADLE resulted in growth inhibition and induction of apoptotic cell death on high-dose as measured by MTT assay and DNA flow cytometer analysis. Bcl-XL, c-IAP-2 and survivin genes especially showed decreases in mRNA levels. DADLE treatment also inhibited the levels of cyclooxygenase (COX)-2 mRNA without alteration of COX-1 expression. DNA flow cytometer analysis revealed that DADLE caused arrest of the cell cycle on low-dose, which was associated with a down-regulation of cyclin E at the transcriptional level. DADLE treatment induced a marked down-regulation of cyclin-dependent kinase (Cdk)-2, -4 and -6. In addition, treatment with DADLE decreased telomere associated genes such as, c-myc and TERT, and increased TEP-1 in U937 cells. These results suggest that DADLE can be an inhibition agent in the cell cycle of the human leukemia cancer U937 cell.

• Environmental Mutagens and Carcinogens
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• v.22 no.2
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• pp.76-82
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• 2002

In human U-937 cell exposed to ${\gamma}$-irradiation and $H_2O$$_2$, the level of mRNA efrpression in ceruloplasmin gene was measured by using comparative RT.PCR (reverse transcriptase-polymerase chain reaction). At the normal growth condition, the level of ceruloplasmin transcript was estimated as 8.2% and 0.0068% of hprt (hypoxantine phosphoribosyl transferase) transcript and of $\beta$-actin transcript, respectively. In U-937 cells exposed to a dose of 100 rad ${\gamma}$-irradiation, the level of ceruloplasmin transcript was increased about 2.7 and 1.6 fold compared to un-treated cell by using compensation with the levels of hprt and $\beta$-actin transcript. By contrast, the expression of ceruloplasmin gene in U-937 cells exposed to $H_2O$$_2$(50 $\mu$M, 24 h), was shown no significant difference compared to un-treated cell. These results indicated that the expression system of ceruloplasmin gene may react only some specific oxygen species, such as reactive oxygen species induced by ${\gamma}$-irradiation.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.2
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• pp.358-364
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• 2006

To investigate the possible mechanism of Drynariae Rhizoma extracts as a candidate of anti-cancer drug, I examined the effects of Drynariae Rhizoma extracts on the apoptosis of U937 cell line. MTT assay, flow cytometric analysis, SDS-polyacrylamide gel electrophoresis, Western blot analysis, and RT-PCR were performed. Drynariae Rhizoma extracts treatment reduced the cell viablilty of U937 cells in a dose-dependent manner, which was associated with induction of apoptotic cell death. Drynariae Rhizoma extracts treatment also reduced the levels of Bcl-xL anti-apoptotic protein expression and increased the levels of caspase-3, p53, pro-apoptotic protein, in U937 cells. RT-PCR data revealed that the level of bcl-2, bcl-xL mRNA expressions decreased in a dose-dependent manner. These findings suggest that Drynariae Rhizoma extracts may have induction of apoptotic cell death via regulation of several growth regulatory gene products. The abbreviations used are: FBS, fetal bovine serum; PBS, phosphate buffered saline; PI, propidium iodide; OD, optical density; DiOC6, 3,3-dihexyloxa carbcyanine iodide; MTT, 3 [4-5-dimethylthiazol-2-yl] -2-diphenyltetrazolium bromide.