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)

Cytokines have various kinds of functions, including immunoregulation, host defense system, induction of inflammation and pathogenesis of many diseases. One of the characteristics of cytokines is the interaction among cytokines, and they further play an important role in the defense against tumor development, although its mechanism is highly complicated. In this paper, cytokines possessing antitumor activity, are described. These are 2 categories of antitumor cytokines, immunological and non-immunological ones. As immunological cytokines, interferons, interleukin 1, 2, 4, 5, 6, 8 and 12, tumor necrosis factor and lymphotoxin, have been investigated. On the other hand, tumor-degenerating factor, tumor regressing factor, glial maturation factor, glial growth inhibitory factor, neuroblastoma growth inhibitory factor, neonatal brain derived carcinostatic factor, chondromodulin and gliostatin have been characterized as non-immunological antitumor cytokines. These cytokines interact, and the complicated network of immunological and non-immunological antitumor cytokines is formed.
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PMID:[Antitumor cytokines]. 143 61

Using a growth factor defined assay for anchorage-independent growth (van Zoelen, E.J.J., van Oostwaard, Th.M.J., van der Saag, P.T. and de Laat, S.W. (1985) J. Cell. Physiol. 123, 151- 160, we have studied the ability of polypeptide growth factors produced by Neuro-2A neuroblastoma cells to induce anchorage-independent growth of normal rat kidney cells. Neuro-2A cells produce and secrete a PDGF-like growth factor in addition to TGF beta, which can be fully separated from each other by means of reverse-phase HPLC. Using a new, very sensitive technique for detection of TGF beta in growth factor samples based on its additional ability to act as a growth inhibitory factor, it is shown that the PDGF-like growth factor does not contain any detectable TGF beta. Still this neuroblastoma derived PDGF-like growth factor is able to induce anchorage-independent growth of NRK cells, particularly in the additional presence of EGF. It is concluded that under growth factor defined assay conditions TGF beta is not essential for phenotypic transformation of NRK cells.
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PMID:PDGF-like growth factor induces EGF-potentiated phenotypic transformation of normal rat kidney cells in the absence of TGF beta. 349 98

Glial growth inhibitory factor (GGIF), derived from the culture medium of mouse neuroblastoma cell (NAs-1), lowered the DNA synthesis and cell multiplication of normal rat glioblasts induced by glia maturation factor (GMF). The inhibitory action of GGIF depended on the concentration of GMF in the culture medium, and was of an uncompetitive type on kinetic analysis. GGIF showed the inhibitory activity at a late stage of the G1 phase or early stage of the S phase. The factor, however, failed to inhibit the differentiation-promoting activity of GMF. The data strongly suggest that the dual activities of GMF, the promotion of glial proliferation and differentiation, may be elicited by mutually independent intracellular processes.
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PMID:Functional dissociation of dual activities of glia maturation factor: inhibition of glial proliferation and preservation of differentiation by glial growth inhibitory factor. 359 69

Growth inhibitory factor for mouse neuroblastoma cells was detected in the culture medium of fetal rat glioblasts, and was partially purified and characterized. The factor had an apparent molecular weight of 75,000 and an isoelectric point of 5.8, and showed no esterase activity. It possessed the activity to promote morphological differentiation including the formation of neural processes and the inhibition of cell division when tested on mouse neuroblastoma cell lines (Neuro 2a, NS-20Y, and NIE-115). The activity was susceptible to protease digestion and heat treatment. The serum over 25% cancelled the inhibitory activity of this factor. The factor failed to increase the intracellular contents of cAMP and cGMP. It showed no effect on either morphological differentiation or proliferation of glial cell lines, suggesting that under physiological conditions the factor acts specifically on neuronal cells.
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PMID:Inhibition of growth of mouse neuroblastoma cels by protein factor derived from rat glioblasts. 628 Aug 7

Neuroblastoma growth inhibitory factor (NGIF) exists in the conditioned medium of normal rat glioblasts. When neuroblastoma cells (Neuro2a, NS-20Y, and N1E-115) were cultured in the presence of the factor, the cell growth rates and DNA synthesis were markedly inhibited and the morphological differentiation including neural process formation was induced. However, the factor neither altered the growth rate nor the morphology of non-neuronal cells such as glial cell lines (C6 and 354A) or fibroblast (3T3). The molecular weight of the factor was estimated to be 75,000 Mr by gel filtration with Bio-Gel P-200, and the isoelectric point was 5.8. The factor was devoid of esteropeptidase activity, and susceptible to protease and thermal treatment. The growth inhibitory action of the factor was unrelated to the intracellular contents of cyclic AMP and GMP. The ability of NGIF to suppress preferentially the neural growth suggests its regulatory role in normal brain development.
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PMID:Characterization and partial purification of neuroblastoma growth inhibitory factor from the culture medium of glioblasts. 629 69

Investigations on the general characteristics of human astrocytoma cell line NAC-1 revealed neuroblastoma growth inhibitory activity in conditioned medium. Neuroblastoma growth inhibitory factor (NGIF) was partially purified by Econo Q, Econo CM, and Superose 12 column chromatography. The protein is weakly basic with an estimated M(r) of 120,000, possibly having an M(r) 60,000 dimeric structure. NGIF inhibits the growth of human neuroblastoma cell lines but has no effect on morphology nor does it produce any change in the growth of human glioblastoma cell lines. Interestingly, NGIF appears to promote survival and neurite outgrowth of embryonal rat cortical neurons. These neurotrophic properties suggest a role for NGIF in the development of the nervous system.
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PMID:Human neuroblastoma growth inhibitory factor (h-NGIF), derived from human astrocytoma conditioned medium, has neurotrophic properties. 805 39

Metallothionein-3(MT-3), also known as growth inhibitory factor (GIF), is predominantly expressed in central nervous system (CNS). It belongs to the family of metallothionein(MT) but has several unique properties that are not shared by other family members such as MT-1/MT-2. In the past few years, MT-3 had been postulated to be a multipurpose protein which could play important neuromodulatory and neuroprotective roles in CNS besides the common roles of MTs. However, the primary function of MT-3 and the mechanism underlying its multiple functions were not elucidated so far. In present study, human neuroblastoma cell line SH-SY5Y was employed to study the overall cellular protein changes induced by transient transfection of MT-3 gene, based on comparative proteome analysis. Averagely about 750 spots were visualized by Coomassie staining in one 2D gel, in which 17 proteins were shown to display significant and reproducible changes by semiquantitative analysis with ImageMaster 2D Elite software. Among them, 12 proteins were up-regulated while other 5 proteins were down-regulated. Using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry, 10 proteins were further identified to be zinc finger protein, glutamate transporter, and enhancer protein, etc., which were involved in several important pathways regulating the functions of central nervous system. The results showed that MT-3 might exert its unique functions by regulating the expression of these proteins.
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PMID:Differential protein expression induced by transient transfection of metallothionein-3 gene in SH-SY5Y neuroblastoma cell line. 1279 12

Effects of thimerosal and its metabolites, ethyl mercury and thiosalicylate, on the expression of metallothionein (MT) mRNAs in mouse cerebellum microglia cell line, C8-B4 cells, were studied. The level of MT-1 mRNA significantly decreased at early hours and recovered time-dependently 24h after thimerosal was added to the C8-B4 cells. However, MT-2 and MT-3 mRNA expressions did not change from the control group. In contrast, the expression of MT-1 mRNA increased in a mouse neuroblastoma cell line 6h after incubation with thimerosal. In addition, the level of MT-1 mRNA decreased in C8-B4 cells 6h after the addition of thiosalicylate, but ethyl mercury induced MT-1 mRNA expression. When cell viability was compared with thimerosal, thiosalicylate, and ethyl mercury, the viability of C8-B4 cells decreased dose-dependently 24h after either thimerosal or ethyl mercury was added; however, the viability increased dose-dependently until 15 microM thiosalicylate was added. From the present results, it is concluded that the expression of MT-1 mRNA may be mediated by different factors than the expression of MT-2 mRNA in C8-B4 cells. The reduction of MT-1 mRNA level by thiosalicylate may affect the proliferation of C8-B4 cells.
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PMID:Expression of metallothionein mRNAs on mouse cerebellum microglia cells by thimerosal and its metabolites. 1938 79

Experimental autoimmune encephalomyelitis (EAE), an animal model for human multiple sclerosis, is characterized by demyelination, inflammation and neurodegeneration of CNS in which free radicals play a role. Recently, the efficacy of murine mesenchimal stem cells (MSCs) as treatment of EAE induced in mice by the encephalitogenic peptide MOG(35-55) was demonstrated. The present study analyzed some markers of oxidative stress, inflammation/degeneration and apoptosis such as metallothioneins (MTs), antioxidant enzymes (superoxide dismutase, catalase and glutathione-S-transferase), poly(ADP-ribose) polymerase-1 and p53 during EAE progression and following MSC treatment. Expression of the three brain MT isoforms increased significantly in EAE mice compared with healthy controls, but while expression of MT-1 and MT-3 increased along EAE course, MT-2 was up-regulated at the onset, but returned to levels similar to those of controls in chronic phase. The changes in the transcription and activity of the antioxidant enzymes and in expression of poly(ADP-ribose) polymerase-1 and p53 showed the same kinetics observed for MT-1 and MT-3 during EAE. Interestingly, i.v. administration of MSCs reduced the EAE-induced increases in levels/activities of all these proteins. These results support an antioxidant and neuroprotective activity for MSCs that was also confirmed in vitro on neuroblastoma cells exposed to an oxidative insult.
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PMID:Neuroprotective mesenchymal stem cells are endowed with a potent antioxidant effect in vivo. 1961 33

A new ascites type neuroblastoma clone (NAs-1), which is characteristic both in anchorage-independent growth and catecholaminergic functions, attached on the monolayer culture of glioblasts and was subjected to morphological differentiation including the extrusion of neuronal processes. Other conventional neuroblastoma cells (Neuro2a, NS-20Y, and N1E-115) as well as NAs-1 in cocultured with normal glioblasts underwent a decrease in cell growth rates and DNA synthesis under the effect of the neuroblastoma growth inhibitory factor (NGIF) produced by glioblasts. After their NGIF production had been reduced by u.v. irradiation, glioblasts lost the growth-inhibitory and differentiation-promoting effects in coculture with NAs-1. The supplement of NGIF into u.v.-treated glioblasts restored the dose-dependent growth inhibition of NAs-1. The addition of nerve growth factor into the coculture system brought about neither the marked effect on growth inhibition of NAs-1 nor the morphological differentiation. The results imply a direct function of NGIF on the paracrine regulation of neuroblastoma cell growth in the coculture with normal glioblasts.
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PMID:Inhibition by neuroblastoma growth inhibitory factor of ascites-type neuroblastoma cell growth in coculture with normal glioblasts. 2049 53


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