Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cell extracts from HeLa, macrophage, glial, C6, PC12, IMR-32, neuroblastoma, CHP-100 and P19 cells were examined for APP and its different derivatives by immunoblotting. When five antibodies (raised against different parts of APP) were used to stain western blots of nine cell extracts, three groups of immunoreactive proteins were observed: high molecular weight-(HMW, 70-125 kDa), medium molecular weight-(MMW, 30-40 kDa) and low molecular weight (LMW, 4-16 kDa). The intensity of immunoreactivity among these three groups of proteins varied in each cell line. The strongest signal for HMW protein was observed in PC 12 cells, the strongest signal for MMW protein was observed in C6 astrocyte cells, and both HMW and MMW protein bands were detected in macrophages and P19 cell lines. LMW protein bands could be detected only by antibody against the carboxyl-terminal part of the APP molecule. These experiments suggest that APP is processed differently in the various cell types. The conversion of APP to beta-peptide may be related to the stability of APP in cells and the understanding of these intermediate steps of APP processing is crucial to the elucidation of Alzheimer's disease.
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PMID:The stability of beta-amyloid precursor protein in nine different cell types. 850 38

alpha-2,8-Sialyltransferase has been purified from human neuroblastoma CHP-134 cells greater than 2900-fold. The key step in the purification was a substrate affinity column utilizing immobilized colominic acid. Several kinetic parameters of the enzyme were defined. Fetuin but not asialofetuin served as substrate. The product of the enzyme reaction was characterized as containing sialyl residues in alpha-2,8-linkage with the use of recombinant sialidases. It is suggested that the purified enzyme is an initiating enzyme for the biosynthesis of polysialic acid since these cells also have the activity of poly alpha-2,8-sialyltransferase and contain polysialic acid. This alpha-2,8-sialyltransferase may be a new member of a family of alpha-2,8-sialyltransferases recently described, since it differs in substrate specificity reported for the cloned and expressed enzymes.
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PMID:Purification of an alpha-2,8-sialyltransferase, a potential initiating enzyme for the biosynthesis of polysialic acid in human neuroblastoma cells. 855 98

We examined the effect of gamma-linolenic acid (GLA) supplementation on the growth and fatty acid composition of three human tumor cell lines (the neuroblastoma CHP-212, the tubal carcinoma TG, and the colon carcinoma SW-620), in order to evaluate the relationship between GLA-induced tumor cell death and the distribution of fatty acids in tumor cells. At the highest GLA concentrations (10 and 20 micrograms/ml), the DNA synthesis was completely abolished; at 5 micrograms/ml GLA only SW-620 cells did not proliferate, while CHP-212 and TG cells showed a residual [3H]-thymidine incorporation. GLA levels were very low in cells grown in control medium; GLA supplementation caused a significant incorporation of GLA itself in all the cell lines at each concentration. In TG and CHP-212 cells, GLA was metabolized, although to a different extent, to dihomo-gamma linolenic acid and arachidonic acid. SW-620 cells neither elongated nor desaturated the incorporated GLA. The highest cytostatic effect was reached when GLA was not transformed into its metabolites, suggesting that the GLA toxicity to tumor cells is not dependent on metabolites but is due to GLA itself.
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PMID:gamma-Linolenic acid supplementation can affect cancer cell proliferation via modification of fatty acid composition. 875 81

In order to clarify the role of cytosolic Ca2+ buffering, a property that in living cells is sustained primarily by high affinity binding proteins, in NMDA receptor-sustained neuron excitotoxicity, cultures of the neuroblastoma line CHP 100 (which is known to express the receptor) were loaded with the chelator BAPTA by incubation with various concentrations (0.03-1 microM) of its acetoxymethylester derivative. The effectiveness of the loading in terms of cytosolic buffering was confirmed by fura-2 measurement experiments in which the [Ca2+]i transients induced by cell exposure to ATP were blunted in the initial peak (up to -75%) and also in the following plateau. When the BAPTA-loaded neuroblastoma cells were exposed to NMDA (1 mM), excitotoxicity was reduced dose-dependently up to almost 70%, while the generation of cGMP was inhibited up to completion. The latter result suggested the possible involvement of nitric oxide in the NMDA-induced excitoxicity, a mechanism confirmed by the dose-dependent inhibitory effect induced by the nitric oxide synthase blocker, L-N-(1-iminoethyl)-ornithine, which protected the cells completely when administered at 300 microM. Flow cytometry analysis of DNA revealed that the mechanism of excitotoxicity in CHP100 cells does not involve apoptosis. We conclude that cytosolic Ca2+ buffering, a property known to vary considerably among neuronal cells and to change in some neurons also during ageing, has a general protective effect. Such a protection appears to take place via the blunting of the glutamate-induced [Ca2+]i responses mediated by the NMDA receptor, with prevention of the ensuing overactivation of nitric oxide synthase and of the irreversible derangement of the ionic homeostasis of the cell.
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PMID:Cytosolic Ca2+ buffering, a cell property that in some neurons markedly decreases during aging, has a protective effect against NMDA/nitric oxide-induced excitotoxicity. 876 26

1. The effects of hypoosmotic stress on cell volume and amino acid efflux were evaluated in the human neuroblastoma cell line CHP-100 with the Coulter Counter Multisizer and radiolabeled amino acid efflux, respectively. 2. CHP-100 cells swelled by approximately 35 +/- 5% (means +/- SE) when the osmolarity of the solution was decreased from 290 to 190 mOsm/kg H2O. The rapid swelling was followed by a biphasic regulatory volume decrease (RVD). 3. In cells loaded with 14C-taurine, hypoosmotic stress induced a 300 +/- 22% (n = 23, P < 0.05) increase in taurine efflux compared with controls. This efflux was inhibited by the chloride channel blockers 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), 4,4'-diisothio-cyanostilbene-2,2'-disulfonic acid (DIDS), niflumic acid and by the volume-activated anion channel blocker tamoxifen. In addition, the swelling-activated taurine efflux was dependent upon extracellular calcium. 4. Similarly, in cells loaded with 14C-glycine, hypoosmotic stress significantly increased glycine efflux, which was also sensitive to NPPB. In contrast, efflux of 3H-glutamate was not significantly altered after hypoosmotic stress. 5. With the use of patch clamp recording techniques, Cl- channels were activated in cell attached patches after exposure to hypoosmotic solutions. 6. In nystatin perforated patches, permeability of the hypoosmotically activated anion channel was observed to be SCN- > I- > Br- > Cl- >> Glutamate. 7. It is concluded that in CHP-100 cells, anion channels are activated during hypoosmotic stress and these channels represent a pathway for efflux of amino acids.
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PMID:Swelling-activated amino acid efflux in the human neuroblastoma cell line CHP-100. 887 Nov 97

Human neuronal cells express neither major histocompatibility complex (MHC) class I RNA nor cell surface molecules but can be induced to do so by various cytokines. In the present studies, we report that expression of MHC class I in a neuroblastoma cell line, CHP-126, is actively repressed. This repression is mediated by the combined effects of a series of upstream silencer elements. Removal of the silencers reveals not only an active promoter element but also the presence of an active enhancer. Four silencers have been identified and shown to have distinct sequences, binding factors, and patterns of function. One element is located between -724 and -697 base pairs (bp) and corresponds to a silencer involved in tissue-specific regulation of class I gene expression. Three additional elements occur between -503 and -402 bp. One of these corresponds to a c-jun responsive element. Neither of the remaining elements corresponds to DNA sequences known to regulate expression of other genes. These data demonstrate that MHC class I expression normally is actively repressed in neuronal cells and suggest a model of rapid and specific triggering of class I in neuronal cells in response to infection.
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PMID:Active repression of major histocompatibility complex class I genes in a human neuroblastoma cell line. 894 88

bcl-x is a member of the bcl-2 family of genes and by alternative splicing gives rise to two distinct mRNAs: bcl-xL and bcl-xS. We have previously investigated the expression of Bcl-x in neuroblastoma (NB) cell lines and have shown that Bcl-xL is expressed and functions to inhibit chemotherapy-induced apoptosis. However, none of the NB cell lines expressed Bcl-xS. The aim of the present study was to determine the effects of Bcl-xS expression on the viability of NB cells. A panel of NB cell lines (CHP-382, GOTO, SHEP-1, SHSY-5Y, and GI-CA-N) were infected with either a bcl-xS adenovirus (pAdRSV-bcl-xS) or a control virus (pAdRSV-lac-z). NB cells showed loss of viability with both viruses, although the bcl-xS virus was most toxic. Importantly, infection with the bcl-xS adenovirus resulted in rapid loss of cell viability, DNA fragmentation, and morphological features of apoptosis even in NB cells transfected to overexpress Bcl-2 and Bcl-xL. These findings suggest that deregulated expression of Bcl-xS using an adenovirus may provide a novel mechanism for initiating cell death in tumors that express Bcl-2 or Bcl-xL.
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PMID:Bcl-xS enhances adenoviral vector-induced apoptosis in neuroblastoma cells. 897 Nov 84

The modulatory effects of neuropeptide Y (NPY) on ATP-induced increases in cytosolic free-calcium concentration ([Ca2+]i) were investigated in the CHP-234 human neuroblastoma cell line. Pretreatment of cells with 100 nM NPY potentiated the increase in [Ca2+]i evoked subsequently by 20 microM ATP, compared with initial application of ATP in a control experiment, whereas a similar pretreatment with 1 microM NPY attenuated the subsequent response to ATP. Both actions of NPY were completely blocked by H-89 [N-[2-((3-(4-bromo-phenyl)-2-propenyl)-amino)-ethyl]-5 isoquinoline sulphonamide dihydrochloride], a selective antagonist of protein kinase A. The effects of 100 nM NPY were mimicked by H-89, while forskolin and 8-Br-cAMP mimicked the effects of 1 microM NPY. Both basal and forskolin-stimulated cAMP levels were inhibited by 100 nM NPY and by 100 nM NPY(13-36), a selective agonist of the NPY Y2-receptor subtype. In contrast, at 1 microM such inhibition was not observed for either NPY or NPY(13-36). It is concluded that NPY has a biphasic modulatory effect on increases in [Ca2+]i produced by ATP, which probably involves the cAMP/protein kinase A cascade.
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PMID:Neuropeptide Y modulates ATP-induced increases in internal calcium via the adenylate cyclase/protein kinase A system in a human neuroblastoma cell line. 902 Aug 78

Amifostine (WR-2721) is currently being investigated as a potential protector of normal tissues during chemotherapy in adult and pediatric cancer patients. The marked reduction of bone marrow and renal toxicity by amifostine is well documented, but data are lacking whether the anticancer activity of cytostatic drugs is also preserved in neuroblastoma as the second most common pediatric malignancy. We investigated the cytotoxic effect of six drugs on two neuroblastoma cells lines chosen for their presence or absence of N-myc amplification and PGY1 overexpression: IMR-5 (N-myc 25 x, PGY1-negative), CHP-100 (N-myc 1x, PGY1-positive) in vitro in the presence and absence of WR-2721 and its active metabolite WR-1065 using the monolayer proliferation assay. Doxorubicin, vincristine, etoposide, cisplatin, 4-hydroperoxycyclophosphamide and 4-hydroperoxyifosfamide were equally cytotoxic with and without preincubation of WR-2721 (14 mM) or WR-1065 (40 microM) as shown by virtually identical dose-response curves and ID50 values. We conclude that WR-2721 and WR-1065 did not reduce the cytostatic activity of six commonly used drugs on neuroblastoma cell lines in vitro.
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PMID:Effects of WR-2721 (amifostine) and its metabolite WR-1065 on the antiproliferative activity of chemotherapeutic agents on neuroblastoma cells in vitro. 914 9

The diverse biological functions of galanin are mediated via membrane bound high-affinity receptors. In order to identify and characterize potential galanin receptor subtypes, we have examined the specific 125I-galanin binding to the CHP-212 human neuroblastoma cell line. The galanin receptors expressed in CHP-212 cells, like GALR1 have high affinity for galanin (Kd = 0.07 nM) and the potency for inhibition of 125I-galanin binding by galanin peptides parallels that of hGALR1 expressed in a stable CHO cell line. We confirmed that GALR1 is expressed in these cells by RT-PCR. We further determined the tissue expression patterns of hGALR1 which is expressed in a variety of human tissues at a very low level, with the highest levels seen in heart, small intestine and prostate. A species of approximately 70 kDa is recognized by antisera specific for hGALR1 by Western blot analysis and should allow future measurements of receptor protein expression.
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PMID:Pharmacological characterization and tissue distribution of the human and rat GALR1 receptors. 916 41


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