Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: KEGG:D02003 (NBT)
 1,323 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Novel vitamin D3 derivatives, 26-homo-delta 22-1 alpha,25(S)-dihydroxyvitamin D3 and 26-homo-delta 22-1 alpha,25(R)-dihydroxyvitamin D3 were compared with the native hormone, 1,25-dihydroxyvitamin D3, and with other vitamin D3 derivatives, in inhibition of cell growth, induction of phenotypic differentiation, and c-myc mRNA reduction of HL-60 cells. The degree of inhibition in cell growth caused by 26-homo-delta 22-1 alpha,25(S)-(OH)2D3 was the greatest followed by 26-homo-delta 22-1 alpha,25(R)-(OH)2D3. The ability to reduce NBT was parallel to that to inhibit cellular proliferation. 26-homo-delta 22-1 alpha,25(S)-(OH)2D3, 26-homo-delta 22-1 alpha,25(R)-(OH)2D3, 24-homo-24-F2-1 alpha,25-(OH)2D3, and 1 alpha,24(R)-(OH)2-26-Cl-D3 were more active than 1 alpha,25-(OH)2D3 in the induction of OK-M1+ and OK-Mo-2+ HL-60 cells. Using two color flow cytometric analysis, the percentages of OK-M5(+)- and OK-DR(+)-HL-60 cells were 33% in the treatment with 26-homo-delta 22-1 alpha,25(S)-(OH)2D3 plus interferon-gamma (IFN-gamma) but 14% in the treatment with 1 alpha,25-(OH)2D3 plus IFN-gamma. 26-Homo-delta 22-1 alpha,25(S)-(OH)2D3 has an inhibitory effect on c-myc reduction in treated HL-60 cells. These results suggest that the novel vitamin D3 derivatives, 26-homo-delta 22-1 alpha,25(S)-(OH)2D3 and 26-homo-delta 22-1 alpha,25(R)-(OH)2D3, have preferential activity in inducing phenotypic differentiation and in inducing cell proliferation related c-myc mRNA activity.
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PMID:Novel vitamin D3 derivatives, 26-homo-delta 22-dehydro-1 alpha,25(S)-dihydroxyvitamin D3 and 26-homo-delta 22-dehydro-1 alpha,25(R)-dihydroxyvitamin D3: preferential activity in c-myc mRNA production and in induction of phenotypic differentiation of HL-60 cells. 240 90

To evaluate the effects of a novel 2-aminosteroid, 2-(4'-methyl-1'-piperazinyl)-3alpha-hydroxyl-5alpha-androstane-17-one (KH), on in vitro murine WEHI-3B leukemia cells, semisolid colony culture, MTT assay, morphological examination, NBT reduction, NSAE test and ACP assay were used to determine proliferation and differentiation. It was found that the growth of leukemia cells in colony and liquid cultures was inhibited by KH (10(-8)-10(-4) mol/l) after treatment for 7 days. The percentages of NBT and NSAE positive cells were 71.17 and 79.25%, respectively, after treatment with KH (10(-8)-10(-6) mol/l) for 5 days. The morphology of treated leukemia cells was identified to be macrophage-like and these cells acquired significant ACP activities. It was indicated that the ACP enzyme activities were increased as high as two and three times of the control, respectively, after treatment with 10(-8) or 10(-5) mol/l KH for 6 days. It was also indicated by DNA fragmentation in gel electrophoresis that WEHI-3B cells were induced toward apoptosis by KH (10(-8)-10(-4) mol/l) when checked at day 5. The c-myc mRNA expressions in WEHI-3B cells were decreased by 58.7% after treatment with KH (10(-8) mol/l) for 5 days. Therefore, it is first reported here that KH, a novel 2-aminosteroid, could suppress proliferation and induce differentiation of WEHI-3B leukemia cells. These differentiated cells were mature macrophage-like cells and showed characteristics of functional phagocytes acquired with acid phosphatase activity. The mechanisms underlying the above effects involved the apoptosis of WEHI-3B leukemia cells and the down-regulation of c-myc oncogene expression. It is also shown that the counts of immature granulocytes and monocytes were significantly decreased in both peripheral blood and bone marrow of BALB/c leukemia mice after KH was administrated per os for 7 consecutive days with four doses (5, 10, 15 or 20 mg/kg day), respectively. It is also observed that the enlarged spleens in leukemia mice were decreased when compared with the control.
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PMID:The effects and mechanisms of a novel 2-aminosteroid on murine WEHI-3B leukemia cells in vitro and in vivo. 1133 17

18:1/docosahexaenoic acid (DHA)-containing phosphatidylethanolamine (PE) enhanced cell differentiation and growth inhibition of HL-60 induced by dibutyryl cAMP (dbcAMP) in a dose-dependent manner. The combined treatment of 200 microM dbcAMP and 50 microM 18:1/DHA-PE increased the NBT reducing activity, which is as an indicator of cell differentiation, to more than 75% from 40% of cells treated with 200 microM dbcAMP alone. In HL-60 cells treated with 50 microM 18:1/DHA-PE and 200 microM dbcAMP for 24 h, the expression level of c-jun mRNA and c-Jun protein were remarkably elevated compared to cells treated with dbcAMP alone. In contrast, there was no difference in the expression levels of c-fos mRNA and c-Fos protein between the combination of 18:1/DHA-PE + dbcAMP or dbcAMP alone. On the other hand, the combine treatment of 18:1/DHA-PE and dbcAMP markedly reduced the expression level of c-myc oncogene during 48 h incubation. The decreases of c-myc mRNA by 18:1/DHA-PE and/or dbcAMP was correlated with growth inhibition effect. Thus, 18:1/DHA-PE might enhance dbcAMP-induced HL-60 cell differentiation and growth inhibition by regulation of c-jun and c-myc mRNA and their products.
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PMID:Docosahexaenoic acid-containing phosphatidylethanolamine enhances HL-60 cell differentiation by regulation of c-jun and c-myc expression. 1633 92