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)

D-Alpha-tocopheryl succinate (vitamin E succinate) at a concentration of 11.3 microM inhibited growth and reduced the expression of c-myc, N-myc and H-ras specific mRNAs in murine neuroblastoma cells (NBP2) in culture. R020-1724 [4-(3-butoxy-4-methoxybenzyl)-2- imidazolidinone], an inhibitor of cyclic AMP phosphodiesterase, also inhibited growth and reduced the expression of these oncogenes. Vitamin E succinate treatment caused the formation of two c-myc related transcript of 1.9 and 3.7 kb; however, R020-1724 treatment did not. These results suggest that the inhibition of growth is sufficient to reduce the expression of c-myc, N-myc and H-ras in NB cells in culture, but it is not sufficient to produce two c-myc related transcripts.
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PMID:Effect of vitamin E succinate and a cAMP-stimulating agent on the expression of c-myc and N-myc and H-ras in murine neuroblastoma cells. 164 46

The effect of alpha-tocopherol (vitamin E) on the proliferation of vascular smooth muscle cells (A7r5), human osteosarcoma cells (Saos-2), fibroblasts (Balb/3T3), and neuroblastoma cells (NB2A) has been studied. The proliferation of vascular smooth muscle cells was inhibited by physiologically relevant concentrations of alpha-tocopherol, neuroblastoma cells were only sensitive to higher alpha-tocopherol concentrations, and proliferation of the other cell lines was not inhibited. The inhibition of smooth muscle cell proliferation was specific for alpha-tocopherol. Trolox, phytol, and alpha-tocopherol esters had no effect. Proliferation of smooth muscle cells stimulated by platelet-derived growth factor or endothelin was completely sensitive to alpha-tocopherol. If smooth muscle cells were stimulated by fetal calf serum, proliferation was 50% inhibited by alpha-tocopherol. No effect of alpha-tocopherol was observed when proliferation of smooth muscle cells was stimulated by bombesin and lysophosphatidic acid. The possibility of an involvement of protein kinase C in the cell response to alpha-tocopherol was suggested by experiments with the isolated enzyme and supported by the 2- to 3-fold stimulation of phorbol ester binding induced by alpha-tocopherol in sensitive cells. Moreover, alpha-tocopherol also caused inhibition of protein kinase C translocation induced by phorbol esters and inhibition of the phosphorylation of its 80-kDa protein substrate in smooth muscle cells. A model is discussed by which alpha-tocopherol inhibits cell proliferation by interacting with the cytosolic protein kinase C, thus preventing its membrane translocation and activation.
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PMID:Inhibition of cell proliferation by alpha-tocopherol. Role of protein kinase C. 200 76

The effects of DL-alpha-tocopherol and DL-alpha-tocopherol succinate on neuroblastoma N1E 115 cells were studied. Tocopherol had no growth-arresting properties, whereas its succinate ester derivative inhibited growth at concentrations greater than or equal to 20 microM. The succinate derivative was taken up somewhat more readily than free tocopherol; however, for any equal uptake of both forms of vitamin E, only the succinate derivative could affect growth. Tocopherol succinate was taken up without marked conversion to tocopherol. Following uptake, plasma membrane and organelle fractions contained most of the vitamin E derivatives; however, the particulate and membrane fractions were about twice as enriched in the succinate derivative as in free tocopherol. On the other hand, a proportionally higher amount of unconjugated vitamin E was recovered in the cytosol fraction. Fluorescence polarization studies indicated no differences in the overall fluidity of the plasma membranes treated or not treated with either form of vitamin E. The data point to the functionality of the free carboxyl group of the succinate derivative as a basis for the difference in potency of the two forms of vitamin E.
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PMID:Studies on the effects of vitamin E on neuroblastoma N1E 115. 271 Jun 49

Two human neuroblastoma cell lines, NCG and GOTO, were used to study the cytotoxic effect of gamma linolenic acid (GLA). The cell growth inhibition of these culture cells by GLA was found to be associated with striking membrane fatty acid modification. When culture cells were exposed to 20 micrograms/ml and 60 micrograms/ml GLA for 48 hr, polyenoic acids in cell membrane phospholipids (PC, PE, PI, PS) and triglyceride significantly increased; 1.8-21.0 fold for NCG and 1.04-11.5 fold for GOTO, in association with decreased monoenoic acids. The most remarkable changes were; increase of C18:3, C20:3, C20:4 and decrease of C18:1. CoQ10 (50 micrograms/ml) and vitamin E (10 microM) shown to protect against the cytotoxic effect of GLA did not modify the incorporation of GLA into tumor cells. These results indicate that the antitumor effect of GLA is probably due to cellular dysfunction caused by fatty acid modification after GLA incorporation.
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PMID:Fatty acid modification of cultured neuroblastoma cells by gamma linolenic acid relevant to its antitumor effect. 282 39

Combined effects of vitamin E (alpha-tocopherol) and cisplatin on the growth of two murine neuroblastomas (C1300, NS-20) was investigated in vivo. Five groups of mice were prepared; group 1 were fed the control diet, group 2 were fed a vitamin E-deficient diet, group 3 were fed a vitamin E-supplemented diet, group 4 were fed the control diet and plus vitamin E solution given intraperitoneally during the treatment (solvent i.p. group), and group 5 were given vitamin E in the same manner (20 mg/kg/day; vitamin E i.p. group). Cisplatin (6 mg/kg) was injected intraperitoneally into the mice of each group during the treatment. In case of the C1300 neuroblastoma, the antitumor activity of cisplatin was most enhanced in the mice receiving vitamin E i.p., and the intra-tumor vitamin E and platinum levels were significantly higher in this group than in the other groups (P less than 0.01, and P less than 0.05 respectively). In contrast, in animals transplanted with the NS-20 murine neuroblastoma, which proved to be a cisplatin-tolerant tumor in separate experiments, no combined effect of those drugs was observed, although the intra-tumor level of platinum was elevated. The possibility was that vitamin E increases the influx of cisplatin into the tumor cells and acts after incorporation of cisplatin through the plasma membrane. Vitamin E did not accentuate the cisplatin-induced renal impairment in vitamin E-loaded groups. Those results suggested that vitamin E should be considered as a co-agent of cisplatin for the treatment of neuroblastoma.
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PMID:Combined effects of vitamin E (alpha-tocopherol) and cisplatin on the growth of murine neuroblastoma in vivo. 320 17

Alpha tocopheryl succinate treatment (6-8 micrograms/ml), which inhibited the growth of murine neuroblastoma (NBP2) cells (46 +/- 3%), reduced basal and prostaglandin (PG)E1- and PGA2-stimulated adenylate cyclase (AC) activity in vitro. It also inhibited sodium fluoride (NaF)- and forskolin-stimulated AC activity, suggesting that the effect of vitamin E succinate on AC activity is mediated via stimulatory GTP-binding protein (Gs) and catalytic subunit. Vitamin E succinate-induced reduction of AC activity is not strictly related to inhibition of cell growth. This is substantiated by the finding that, although retinoic acid and butylated hydroxyanisole reduced the growth by over 50%, they did not inhibit AC activity. On the other hand, 4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone (R020-1724, 200 micrograms/ml), which inhibited growth (73 +/- 3%) and induced differentiation in NB cells, increased basal and PGE1-stimulated AC activity. Vitamin E succinate treatment also reduced PGE1- and PGA2-AC activity in murine fibroblasts (L-cells) without inhibiting growth.
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PMID:Effect of alpha tocopheryl succinate on adenylate cyclase activity in murine neuroblastoma cells in culture. 320 80

The effects of vitamin E (vit.E, d-alpha-tocopherol acid succinate) on the growth and the morphological differentiation of 4 representative murine neuroblastoma cell lines: C1300 (wild type), NS-20 (cholinergic type), N-18 (inactive type), N1E-115 (adrenergic type), and the combined effects of vit.E and cis-diamminedichloroplatinum(II)(cisplatin, CDDP) were studied in culture. Vitamin E inhibited the growth of all clonal cells in a dose-dependent manner, especially that of NS-20 cells, and it caused significant morphological differentiation only in NS-20 cells. In addition, vit.E enhanced the growth inhibition of C1300 cells by cisplatin in an additive manner, but not that of NS-20 cells. These suggested that both phenomena induced by vit.E may not always occur in parallel in each clonal neuroblastoma, and both mechanisms might be different.
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PMID:Different effects of vitamin E on the growth and morphological differentiation of 4 murine neuroblastoma cell lines in vitro. 323 50

Two new neuroblastoma (NB) cell lines, NUB-6 and NUB-7, were established from recurrent and primary NB tumours respectively and identified conclusively as NB by their phenotypic characteristics, catecholamine production and N-myc amplification. The cell lines could be distinguished on the bases of distinctive growth patterns in monolayer culture and semi-solid media (collagen gel and agarose), neurite formation and their response to four classes of growth and differentiation modulators. The NUB-6 cell line consisted of two distinct cell subtypes, small typical neuroblasts and larger spheroid-forming cells, while NUB-7 was homogeneously neuroblastic. Class-I agents (dibutyrl cyclic AMP [dbcAMP], butyrate, and papaverine) inhibited growth of both cell lines, while only dbcAMP stimulated the formation of short neurites by NUB-6 neuroblast cells in monolayer culture and collagen. Of the class-II agents (vitamins), retinoic acid inhibited growth of both cell lines and stimulated formation of long neurites by NUB-6 cells and NUB-7 cells in later passages. In contrast, vitamin E inhibited growth of NUB-6 and late-passage NUB-7, but stimulated early passage NUB-7. The class III agent (nerve growth factor) resembled vitamin E. The class-IV agents (interferons; rIFN-alpha 2a and rIFN-gamma 1) inhibited growth of both cell lines in monolayer culture and agarose, but stimulated NUB-6 neuroblasts and early passage NUB-7 cells to form long neurites. Thus phenotypically distinct NB cell lines were established in vitro and shown to be differentially influenced by various growth and differentiation modulators. The potent effect of IFN suggests a role for these modulators in NB behaviour in vivo.
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PMID:Phenotypic and molecular characterization of inducible human neuroblastoma cell lines. 324 86

The effect of dl-alpha-tocopheryl (vitamin E) succinate in combination with Prostaglandin A2 (PGA2) and sodium butyrate on mouse neuroblastoma cells (NBP2) in culture, according to the criteria of growth inhibition and morphological differentiation (neurite formation), was studied. Results showed that PGA2 and sodium butyrate inhibited the growth of NB cells in a dose-dependent manner. The combined effects of vitamin E succinate with PGA2 or sodium butyrate, according to the criterion of growth inhibition, were additive. Vitamin E succinate by itself did not induce morphological differentiation, but it enhanced PGA2-induced morphological differentiation. Sodium butyrate alone or in combination with vitamin E succinate did not significantly increase the level of morphological differentiation. Sodium succinate and an equal amount of solvent (ethanol) failed to modify the effect of PGA2 or sodium butyrate. This suggests that the effect of vitamin E succinate in modifying the response of PGA2 and sodium butyrate on NB cells is due to the effect of vitamin E rather than to that of succinate.
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PMID:Effects of dl-alpha-tocopheryl succinate in combination with sodium butyrate and cAMP stimulating agent on neuroblastoma cells in culture. 609 78

The effect of heat in combination with DL-alpha-tocopheryl (vitamin E) succinate and adenosine 3', 5'-cyclic monophosphate (cAMP) stimulating agents on mouse neuroblastoma cells ( NBP2 ) in culture on the criterion of growth inhibition (due to cell death and inhibition of cell division) was studied. Heat (41 degrees-40 degrees) alone inhibited growth; however, the extent of growth inhibition was dependent upon the temperature and the time of heat treatment. Heat (41 degrees-40 degrees) in combination with vitamin E succinate (5 micrograms/ml) produced an additive effect on the criterion of growth inhibition. Vitamin C (100 micrograms/ml) failed to modify the effect of heat. Prostaglandin A2, a stimulator of adenylate cyclase, and 4 - (3-butoxy-4-methoxybenzyl)-2-imidazolidinone ( R020 -1724), an inhibitor of cyclic nucleotide phosphodiesterase, are known to induce irreversible differentiation in mouse neuroblastoma cells in culture. These agents, in combination with heat (40 degrees) produced a synergistic effect on the criterion of growth inhibition. These data suggest that the addition of vitamin E and cAMP stimulating agents may increase the effectiveness of hyperthermia protocol.
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PMID:Effect of hyperthermia in combination with vitamin E and cyclic AMP on neuroblastoma cells in culture. 632 55


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