amanitins and Neuroblastoma
amanitins has been researched along with Neuroblastoma* in 5 studies
Other Studies
5 other study(ies) available for amanitins and Neuroblastoma
Article | Year |
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Induction of catecholamine synthesis in human neuroblastoma cells by replication inhibitors and sodium butyrate.
Various inhibitors of DNA synthesis induced neurite extension in human neuroblastoma cells. In order to clarify morphology-function relationship in differentiation of neuroblastoma cells, the effect of the replication inhibitors on inducibility of catecholamine synthesis was examined. The reagents alone did not affect production of dopamine and noradrenaline, but joint administration of each inhibitor and sodium butyrate considerably promoted the catecholamine synthesis, without additional change in neurite profile. Although inactive in neurite extension, sodium butyrate was moderately active in catecholamine production. The promoting effect of thymidine (or hydroxyurea) and sodium butyrate was repealed by alpha-amanitin, actinomycin D or cycloheximide. Topics: Amanitins; Antineoplastic Agents; Butyrates; Cyclic AMP; Cycloheximide; Dactinomycin; DNA Replication; Dopamine; Homovanillic Acid; Humans; Hydroxyurea; Kinetics; Neuroblastoma; Norepinephrine; Thymidine; Tumor Cells, Cultured; Tyrosine 3-Monooxygenase; Vanilmandelic Acid | 1999 |
The plasma membrane NADH-diaphorase is active during selective phases of the cell cycle in mouse neuroblastoma cell line NB41A3. Its relation to cell growth and differentiation.
Plasma membrane oxidoreductases have been described in all cells and use extracellular impermeant electron acceptors (DCIP, Ferricyanide) that are reduced by NADH. They appear to regulate the overall cell activity in response to oxidative stress from the cellular environment. An NADH-DCIP reductase has been described at the plasma membrane of NB41A3, a neuroblastoma cell line (Zurbriggen and Dryer (1993) Biochim. Biophys. Acta 1183, 513-520) whose activation with extracellular impermeant substrates promotes cell growth. Elutriation was performed to separate cells and the various fractions were analysed for enzyme activity on intact cells combined with flow cytometry. These studies showed that the enzyme is mostly induced and activated during the G1 and during the G2/M-phases. These observations were further corroborated with specific inhibitors of the cell cycle. A three-fold increase in enzyme activity was observed in the presence of alpha-amanitin, a specific cell cycle inhibitor of the G1-phase. Taxol, a specific inhibitor of the M-phase, also induces a significant increase in enzyme activity. FACS analysis of taxol -treated and alpha-amanitin-treated cells corroborated these data. The cells have been synchronized and the enzyme activity was measured at different time intervals. An activity increase was observed after ca. 2-3 h, that corresponds to a raise in the M-phase, according to FACS data. Furthermore, NTera-2 cells - a human neuroblastoma cell line that differentiates into fully mature neurones in the presence of retinoic acid - exhibit a 50% decrease in the enzyme activity during the G0-phase upon differentiation, compared to undifferentiated cells. Together the data presented in this paper show that this plasma membrane NADH-diaphorase affects cell growth and differentiation and is strongly modulated at various phases of the cell cycle. Topics: Amanitins; Animals; Cell Cycle; Cell Differentiation; Cell Division; Cell Line; Cell Membrane; Dihydrolipoamide Dehydrogenase; Flow Cytometry; Humans; Kinetics; Mice; Neuroblastoma; Paclitaxel; Time Factors; Tumor Cells, Cultured | 1996 |
Electron microscopic localization of acridine orange binding to euchromatin in human neuroblastoma cells.
The purpose of the present study was to examine the distribution pattern of acridine orange (AO) chromatin interaction products (AOCI) in human neuroblastoma IMR-32 cells and to test whether AO labeling is correlated with BrdU incorporation, and immunohistochemical localization of DNA polymerase alpha, and human N-myc-gene product. Effects of aphidicolin, alpha-amanitin, and actinomycin D on visualization of AO binding to euchromatin and on N-myc-gene expression were also examined. About 25% of the cell nuclei in logarithmic growth phase were immunohistochemically demonstrated to be labeled with BrdU after incubation at 37 degrees for 30 min, indicating cells in DNA synthesis. Most of the cell nuclei showed positive immunoreactivity to DNA polymerase alpha, while human N-myc gene product was found in about 60-80% of the cell nuclei. Electron microscopic studies revealed that about 25% of neuroblastoma cells showed characteristic AOCI within cell nuclei. In the presence of aphidicolin, alpha-amanitin, and actinomycin D, positive cells for N-myc gene product decreased markedly. Percentages of AO positive cells and numbers of AOCI per cell nucleus also showed a marked decrease. But northern blot analysis demonstrated that the expression level of N-myc gene was only repressed by the transcriptional inhibitors alpha-amanitin and actinomycin D. However, no repression was caused by aphidicolin. The present and previous studies of the authors suggest that the ultracytochemical AO method may be indicative for conformational changes of chromatin of cells confined to the cell cycle. Inhibitors of RNA and DNA synthesis then may change the conformational state of chromatin.(ABSTRACT TRUNCATED AT 250 WORDS) Topics: Acridine Orange; Amanitins; Aphidicolin; Blotting, Northern; Bromodeoxyuridine; Cell Nucleus; Chromatin; Dactinomycin; Diploidy; Diterpenes; DNA Polymerase II; DNA, Neoplasm; Euchromatin; Flow Cytometry; Gene Expression Regulation, Neoplastic; Genes, myc; Humans; Immunohistochemistry; Microscopy, Electron; Neuroblastoma; Proto-Oncogene Proteins c-myc; Tumor Cells, Cultured | 1991 |
A cell line with decreased sensitivity to the methyl mercury-induced stimulation of alpha-amanitin sensitive RNA synthesis in isolated nuclei.
1. In nuclei isolated from cells of the B50 rat neuroblastoma line the stimulatory effect of methyl mercury on alpha-amanitin-sensitive RNA synthesis is very much reduced compared to the stimulatory effect in HeLa nuclei (see: Frenkel G. D. and Randles K. (1982) Specific stimulation of alpha-amanitin-sensitive RNA synthesis in isolated HeLa nuclei by methyl mercury. J. biol. Chem. 257, 6275-6279). 2. The stimulatory effect of another mercury compound, p-hydroxymercuribenzoate, was also much less pronounced in the B50 nuclei. 3. Similar results were obtained with nuclei isolated from B50 cells which had been induced to differentiate by exposure to dibutaryl cyclic AMP. 4. Nuclei isolated from cells of another rat neuroblastoma line (B35), and nuclei from cells of a human neuroblastoma line both exhibited levels of stimulation similar to that of HeLa nuclei. 5. The B50 and HeLa cells were also compared as to their sensitivity to other effects of methyl mercury. Topics: Amanitins; Cell Line; Cell Nucleus; Drug Resistance; HeLa Cells; Humans; Hydroxymercuribenzoates; Methylmercury Compounds; Neuroblastoma; RNA, Neoplasm; Tumor Cells, Cultured | 1988 |
Cycloheximide reduces PGD2 or delta 12-PGJ2 cytotoxicity on NCG cells.
To study the precise mechanism of cytotoxic activity of PGD2 or delta 12-PGJ2 (a biologically active metabolite of PGD2), we examined the effect of various compounds on PGD2 or delta 12-PGJ2 cytotoxicity, using a human neuroblastoma cell line (NCG). Cycloheximide (CHM) specifically protected PGD2 cytotoxicity on NCG cells. When delta 12-PGJ2 was tested, CHM exhibited a similar rescue effect. Puromycin, mitomycin C, and alpha-amanitin did not affect PGD2 or delta 12-PGJ2 cytotoxicity. Emetine showed a variable and no consistent rescue effect CHM may have been active at the primary site where PGD2 or delta 12-PGJ2 exerts its cytotoxicity. This is the first report indicating that CHM reduces the cytotoxicity induced by PGD2 or delta 12-PGJ2. Topics: Amanitins; Cell Line; Cell Survival; Cycloheximide; Drug Interactions; Emetine; Humans; Mitomycin; Mitomycins; Neuroblastoma; Prostaglandin D2; Prostaglandins D; Puromycin | 1986 |