Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001418 (adenocarcinoma)
 68,496 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antiproliferative effects of various calcium-modifying agents were investigated in human AGS gastric carcinoma cells in culture. Variation of the extracellular calcium concentration, achieved by addition of calcium to the growth medium or binding of calcium to the calcium-chelating agent EDTA, appeared to have little influence on growth of the tumor cells. In contrast, the calcium antagonist verapamil, the calcium ionophore A 23.187 and the calmodulin antagonist W 7, agents supposed to interfere with the regulation of the intracellular calcium concentration, all exerted marked growth inhibiting effects. Our results provide evidence for an important role of intracellular calcium-dependent mechanisms in growth regulation of the human gastric adenocarcinoma cell line AGS.
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PMID:Effect of calcium-modifying agents on the growth of human gastric carcinoma cells in vitro. 144 22

Human stomach adenocarcinoma (AGS), astrocytoma (AST) and myelogenous leukemia (K562) cells were co-cultured with human peripheral blood leukocytes (PBL) through four days. Histamine releasing activity (HRA, lymphokines that stimulate degranulation of basophilic leukocytes with the release of histamine) and interferons alpha and gamma (IFN alpha and IFN gamma) were detected in the culture fluids. Maximal levels of HRA were detected by 24 hr in AST and K562-leukocyte co-culture fluids. Notably, only low levels of HRA was detected in AGS-leukocyte cultures. HRA was separated into two molecular weight species (60,000 and 25,000) by column chromatography. The IFN activity was shown to be a mixture of IFN alpha and IFN gamma (IFN alpha greater than IFN gamma). IFN did not cause histamine release from human PBL or affect HRA. Our results indicate that PBL from normal individuals produce HRA in response to tumor antigen and suggest that the basophilic leukocyte response to certain cancers may be related to HRA production.
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PMID:Histamine releasing activity (HRA) produced by leukocytes co-cultured with tumor cells. 244 99

The relative enhancing effects of hyperthermia on the three types of interferon were evaluated in cloning studies for three human cell lines: G-361 malignant melanoma cells, WISH ammion cells, and AGS stomach adenocarcinoma cells. Hyperthermia enhanced the antiproliferative activity of rHuIFN-gamma against each of the three cell lines and the levels of enhancement by hyperthermia were seen to increase with increasing concentrations of rHuIFN-gamma. The maximum observed levels of enhancement of rHuIFN-gamma activity by hyperthermia varied from cell line to cell line. However, when the relative sensitivities of the cell lines to rHuIFN-gamma were taken into account, the levels of enhancement of rHuIFN-gamma antiproliferative activity by hyperthermia were seen to be similar for each of the cell lines, indicating that hyperthermia consistently enhanced rHuIFN-gamma antiproliferative activity. Hyperthermia did not consistently enhance the antiproliferative activities of HuIFN-alpha and HuIFN-beta. Further studies indicated that hyperthermia enhanced by approximately 6-fold the antiproliferative effects of combinations of rHuIFN-gamma with HuIFN-alpha and HuIFN-beta. The results support the possibility that a combination treatment protocol of hyperthermia and interferon administration (particularly HuIFN-gamma or combinations of HuIFN-gamma with HuIFN-alpha or HuIFN-beta) may provide an enhanced antitumor effect in man.
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PMID:Effects of hyperthermia on the in vitro antiproliferative activities of HuIFN-alpha, HuIFN-beta, and rHuIFN-gamma employed separately and in combination. 315 Nov 43

Helicobacter pylori is a bacterial pathogen of humans that infects the gastric mucosa. This infection has been associated with gastritis, peptic ulcers, and gastric carcinomas. Diverse in vitro studies have described efficient adherence of H. pylori to different types of epithelial cells. Because of its varied effects on host cells, we have analysed signal transduction events in H. pylori-infected epithelial cells. Our results show that H. pylori induces an increase in inositol phosphates in all cultured epithelial cells used, including HeLa, Henle 407, Hep-2, and the human gastric adenocarcinoma cell line AGS. Bacterial growth medium supernatants induce a similar response in the host cell. The increase in inositol phosphates is not related to redistribution of cytoskeletal proteins such as actin or alpha-actinin nor tyrosine-phosphorylation of host cell proteins. The inositol phosphate increase is also observed in cells infected with low or non-adherent H. pylori mutants or mutants defective in the vacuolating toxin or urease holoenzyme. These results indicate that inositol phosphate release in H. pylori-infected cells is not dependent on bacterial adherence, and that a soluble bacterial factor, but not the vacuolating toxin or urease holoenzyme, mediates such an effect.
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PMID:Helicobacter pylori induces an increase in inositol phosphates in cultured epithelial cells. 760 12

The purpose of this study was to assess the efficacy of verapamil (20 microM) and hyperthermia (42 degrees C) as modifiers of mitomycin C (MMC), used at different concentrations, in inhibiting the growth of human gastric adenocarcinoma (AGS) cells. Combined verapamil and hyperthermia treatment resulted in a significant decrease in cell count by 72.2% as compared with the control value. Verapamil drastically enhanced the growth-inhibitory activity of MMC at high concentration against AGS cells by 67.5% and had no effect at intermediate and low concentrations. Hyperthermia did not enhance the effect of MMC on AGS cells. The modalities analyzed in this study require further investigation and may have potential for in vivo studies on gastric cancer therapy in the near future.
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PMID:Effect of mitomycin C, verapamil, and hyperthermia on human gastric adenocarcinoma. 800 60

Four full-length cDNA clones coding for preprocathepsin B were isolated from a human gastric adenocarcinoma cDNA library (AGS 1-6-30-1) and analyzed for possible sequence modifications that might be linked to altered intracellular trafficking and secretion of cathepsin B (CTSB) in malignant tumors. Comparison of AGS 1-6-30-1 cDNAs with human kidney/hepatoma cDNAs revealed: (1) three potential N-glycosylation sites instead of two, (2) a nucleotide (nt) substitution in the coding region for the propeptide from GTG to CTG which would result in a Val26-->Leu change, (3) three silent nt replacements in the coding region for the mature protein, (4) five single-nt differences in the 5'- and 3'-UTR (untranslated regions), (5) heterogeneity in the 5'-UTR, and (6) a 10-bp insertion in the 3'-UTR. The 10-bp insertion in the 3'-UTR may alter the stability of CTSB mRNA transcripts and thereby the expression of CTSB. These clones should be useful for expressing human tumor CTSB and analyzing the function of this enzyme in malignant progression. Two restriction-fragment length polymorphisms (RFLPs), EcoRI and TaqI, were detected by Southern blot analysis of genomic DNA from 36 unrelated Caucasians. Inheritance and distribution of the EcoRI alleles (13.0 and 11.0 kb) and the TaqI alleles (5.7 and 4.6 kb) indicated they were independent polymorphisms. In contrast to the EcoRI alleles of 13.0 and 11.0 kb observed in the population survey, genomic DNA from two AGS gastric adenocarcinoma subclones revealed two EcoRI alleles of 13.0 and 7.8 kb.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Human gastric adenocarcinoma cathepsin B: isolation and sequencing of full-length cDNAs and polymorphisms of the gene. 811

Exogenous gastrin exerted a trophic effect on the human gastric adenocarcinoma cell line AGS with a maximum stimulation at 100 pM. The CCK/gastrin receptor antagonists proglumide and loxiglumide dose-dependently inhibited spontaneous growth of AGS gastric cancer cells with half maximal inhibition at 8 mM and 200 microM, respectively. This growth inhibition could not be reversed by coincubation with gastrin. In control experiments with murine 3T3 fibroblasts gastrin had no growth-promoting effect. Proglumide and loxiglumide, however, exerted the same growth inhibition on 3T3 cells as they did on gastrin-responsive AGS tumor cells, suggesting a gastrin receptor independent mode of action. L 365, 260 had no effect on the spontaneous growth of AGS tumor cells, but abolished growth stimulation by exogenous gastrin in a dose-dependent manner. These results suggest that only the high-affinity gastrin receptor antagonist L 365, 260 acts by a specific, i.e. selective, reversible, and competitive mode of action. In contrast, the low affinity CCK/gastrin receptor antagonists proglumide and loxiglumide obviously have an irreversible and non-competitive mode of action with respect to growth inhibition of AGS gastric cancer cells, which is not mediated by gastrin receptors.
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PMID:Differential mode of action of high- and low-affinity CCK/gastrin receptor antagonists in growth inhibition of gastrin--responsive human gastric adenocarcinoma cells in vitro. 831 2

A cDNA for procathepsin E was generated from human gastric adenocarcinoma (AGS) cells, amplified by PCR and inserted into the T7 dependent vector pET 22b for expression in E. coli. Purification of the resultant product was accomplished simply, without the need to resort to column chromatography. The recombinant protein displayed comparable properties to those of its naturally occurring counterpart. The yield of homogeneous active enzyme obtained was approximately 3 mg per 40 g of cells. This is sufficient to permit crystallisation and structural analysis to begin and a mutagenesis programme to examine structure/activity relationships now to be undertaken.
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PMID:Human cathepsin E produced in E. coli. 832 57

In the human gastric adenocarcinoma cell line AGS the effects of the protein-kinase-C-activating phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA), the protein kinase C inhibitor staurosporine, the adenylate-cyclase activating agent forskolin, and the permeable dibutyryl-adenosine 3',5'-monophosphate (Bt2cAMP) on the proliferation were assessed. Cell counting followed 5 days of incubation. Prolonged activation of protein kinase C by TPA, inhibition of protein kinase C by staurosporine, activation of adenylate cyclase by forskolin or a direct increase of the intracellular cAMP level all result in a dose-dependent growth inhibition of AGS gastric tumour cells. Half-maximal inhibition was achieved at 100 pM for TPA, 1 nM for staurosporine, 20 microM for forskolin, and 600 microM for Bt2cAMP. It is concluded that protein kinase C and adenylate cyclase play a fundamental role in the growth of AGS gastric cancer cells. Interference with these enzymes involved in the signal transduction of growth regulation in tumour cells may represent a target in the development of new antiproliferative principles.
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PMID:Protein kinase C and adenylate cyclase as targets for growth inhibition of human gastric cancer cells. 840 80

Many Helicobacter pylori strains produce a cytotoxin (VacA) that induces vacuolation in epithelial cells. In this study, binding and internalization of the cytotoxin by HeLa or AGS (human gastric adenocarcinoma) cells were characterized by indirect fluorescence microscopy. Cells incubated with the cytotoxin at 4 degrees C displayed a uniform fluorescent plasma membrane signal. Preincubation of the cytotoxin with either rabbit antiserum to approximately 90-kDa H. pylori VacA or sera from H. pylori-infected persons inhibited its binding to cells and blocked its capacity to induce cytoplasmic vacuolation. Recombinant VacA fragments (approximately 34 and approximately 58 kDa), corresponding to two proteolytic cleavage products of approximately 90-kDa VacA, each bound to the plasma membrane of HeLa cells. Antiserum reactive with the approximately 58-kDa VacA fragment inhibited the binding of native H. pylori cytotoxin to cells and inhibited cytotoxin activity, whereas antiserum to the approximately 34-kDa fragment had no effect. When incubated with cells at 37 degrees C for > or = 3 h, the H. pylori cytotoxin localized intracellularly in a perinuclear location but did not localize within cytotoxin-induced vacuoles. When cells with previously bound cytotoxin were incubated with anticytotoxin serum at 4 degrees C and then shifted to 37 degrees C, vacuolation was completely inhibited. Bound cytotoxin became inaccessible to the neutralizing effects of antiserum after 60 to 120 min of incubation with cells at 37 degrees C. These data suggest a model in which (i) VacA binds to cells primarily via amino acid sequences in its 58-kDa fragment, (ii) VacA internalization occurs slowly in a temperature-dependent process, and (iii) VacA interacts with an intracellular target.
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PMID:Binding and internalization of the Helicobacter pylori vacuolating cytotoxin by epithelial cells. 892 88


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