Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A cell line (HGC-27) was established by culture of the metastatic lymph node from a gastric cancer patient diagnosed histologically as undifferentiated carcinoma. HGC-27 cells were polygonal or short spindle-shaped and adhered to glass surfaces as a monolayer. The cells were probably derived from gastric cancer cells, as their origin from mesenchymal tissues can be excluded morphologically and enzyme-histochemically. Enzyme activities were generally negative or low, except for adenosine triphosphatase, lactic dehydrogenase and leucine aminopeptidase. These scanty findings might reflect the undifferentiated character of the original tumor cells. The cloning efficiency was 5.3% in liquid medium and 1.0% in soft agar. The doubling time was about 17 hr. Chromosomal analysis revealed a mode of 109 and 110 chromosomes.
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PMID:Human cell line (HGC-27) derived from the metastatic lymph node of gastric cancer. 13 73

Plasma membrane-associated adenosine triphosphatase (ATPase) samples partially purified from the tumor dissections of 15 gastric cancer patients were examined for sensitivity to the synthetic lignan, 2,3-dibenzylbutane-1,4-diol (hattalin), and ouabain in the presence of Mg2+, Na+, and K+. Hattalin was the strongest Na+, K(+)-ATPase inhibitor among the lignans previously examined. The enzyme from normal gastric tissue of the same patient was used as control. The specific activity of ATPase from cancer tissue (C-ATPase) was inhibited by more than 50% by 2.0 mM hattalin, whereas only 33.1% of the specific activity of ATPase from normal gastric mucosa (N-ATPase) was inhibited by 2.0 mM hattalin. There was statistical significance of lignan sensitivity between C- and N-ATPase (p less than 0.02). Ouabain also inhibited C-ATPase in preference to N-ATPase, though not significantly. Hattalin inhibited both C- and N-ATPase more strongly than did ouabain (p less than 0.05). Moreover, the lignan inhibited both C- and N-ATPase in the absence of Na+ and K+. From these data, it is evident that the sensitivity of plasma membrane-associated to lignan increased by gastric canceration. The target ATPase of hattalin is likely to be one other than sodium- and potassium-dependent, ouabain-sensitive ATPase.
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PMID:Differential sensitivity of human gastric cancer ATPase and normal gastric mucosa ATPase to the synthetic mammalian lignan analogue 2,3-dibenzylbutane-1,4-diol (hattalin). 183 Aug 24

N-Nitrosamine formation by bacteria in the achlorhydric stomach has been proposed as an important factor in the development of gastric cancer. Thus, the effect of the presence of bacteria in the stomach on endogenous nitrosation was investigated in rats given omeprazole (an inhibitor of gastric H+, K((+)-ATPase) which reduces gastric secretion sufficiently to allow survival of a bacterial suspension of Escherichia coli or Pseudomonas. When rats were given both thiazolidine 4-carboxylic acid and nitrate, greater endogenous nitrosamine formation was observed in rats receiving omeprazole and an E. coli suspension than in control or omeprazole-treated rats. A similar result was obtained when rats were given morpholine and nitrate. Since the endogenous formation of N-nitrosomorpholine (NMOR) can be evaluated more precisely from the levels of its urinary metabolites, N-nitrosohydroxyethylglycine (NHEG), the metabolism of NMOR was studied in omeprazole-treated rats. In this preliminary study, we showed that 60% of an oral dose of NMOR was excreted as NHEG, while in rats with a higher gastric pH 20% was excreted as NHEG. The amount of endogenously formed NMOR was increased in omeprazole-treated rats given morpholine and nitrite together with bacteria, and greater excretion of unchanged urinary NMOR was observed. Thus, as shown in this in-vivo model, bacteria efficiently reduce nitrate to nitrite and catalyse nitrosation, resulting in increased endogenous formation of N-nitroso compounds in the achlorhydric stomach.
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PMID:Bacterial formation of N-nitroso compounds in the rat stomach after omeprazole-induced achlorhydria. 185 48

This paper describes the cellular and tissue distribution of P-glycoprotein (P-GP) (mdr1 gene product), the role of P-GP in vivo and immunodiagnosis of multi-drug-resistant cancers. We mainly used MRK 16 monoclonal antibody (MAb) reactive with P-GP. P-GP was found to be expressed very strongly in the adrenal cortex of adults and strongly in the renal tubules of the kidney, capillary blood vessels of the brain, and also in placenta. Interestingly, P-GP was not distributed in fetal and neonatal adrenals, and thus may be closely related to adrenal maturation. A high level of P-GP expression was also seen in all cases of functional hormone-producing adrenal tumor, one case of insulinoma, two cases of untreated colonic cancer, one case each of untreated lung cancer, gastric cancer and breast cancer, six cases of renal cell carcinoma and 17 cases of bladder cancer. Using flow cytometry and immunocytochemistry, we investigated the reactivity of MRK 16 MAb with peripheral human mononuclear cells (mainly blastic cells and lymphocytes) from 31 patients with leukemia or malignant lymphoma. Reactivity with MRK 16 MAb was observed in five cases. Some cases reflected the prior administration of adriamycin, vincristine and VP-16, which are known to induce P-GP expression. P-GP-MRK 16-protein A-Sepharose complex derived from human adrenal possessed marked ATPase activity. These data suggest that P-GP may play a physiological role in the human adrenal. Finally, diagnostic criteria of multi-drug-resistant cancers are presented.
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PMID:Expression and functions of P-glycoprotein (mdr1 gene product) in normal and malignant tissues. 197 61

This paper describes the characteristics of exotoxins produced by Helicobacter pylori, and in particular the vacuolating toxin (VacA) and the cytotoxin-associated protein (CagA). The possible association between infection by strains of certain phenotypic or genomic types and the seriousness of gastroduodenal diseases is discussed. Helicobacter pylori induces various morphological changes in cells in vitro, but only infection by strains which induce cytovacuolation has been studied at present. In its native form, VacA is a protein aggregate made of subunits with a mass of 95 kDa. In vitro it stimulates a cellular v-type ATPase present on the endosomes and creates an acidic environment inside the vacuoles. It also alters in vitro a K(+)-dependent phosphatase activity and could impair the flux of sodium through the cells. Purified VacA causes ulceration in mice; experimental infection in mice with strains which also express the CagA protein causes gastric erosions, vacuolation and epithelial and stromal polymorphonuclear (PMN) cell infiltration. In vivo vacuolation can be observed in gastric cells from patients infected with type I (VacA-CagA positive) H. pylori. CagA is a protein of 128-140 kDa molecular weight, noncytotoxic and highly immunogenic. It is coexpressed in approximately 70% of cytotoxin-producing strains. In CagA positive strain infection, increased levels of interleukin-8 (IL-8) are secreted by the colonized gastric mucosa. Patients infected by cytotoxic strains and/or patients with anti-CagA antibodies are more likely to have active gastritis, and are more likely to develop peptic ulcer or gastric cancer. The different outcomes of infection could be determined by host factors, diet, or by the age at which infection is acquired.
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PMID:Helicobacter pylori exotoxins and gastroduodenal diseases associated with cytotoxic strain infection. 873 Feb 63

Using ATPase reaction Langerhans cells were studied in human epidermis obtained from healthy volunteers, corpses of people who died from trauma and were autopsied during first 3 postmortem hrs and patients operated for inflammatory and oncological diseases of different localization. The extent of Langerhans cells alteration was shown to correlate directly with the severeness of the disease the patients has been operated for. Least changes of Langerhans cells developed in people operated for hernia of the anterior abdominal wall while most pronounced changes were found in those operated for stomach cancer of IV stage. The studying of Langerhans cells may be used in clinical practice for evaluation of efficiency of the treatment and in prognostic purposes.
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PMID:[The morphofunctional changes in the Langerhans cells of the human epidermis in inflammatory and cancerous diseases]. 1070 1

The search for differentially expressed genes in gastric cancer may help define molecular alterations and molecular diagnosis of gastric cancer. Using the differential display PCR technique, we identified 18 genes that are differentially expressed between normal and tumor human gastric tissues. Their expressions were verified with reverse Northern blot analysis and Northern blot analysis. Oxidative phosphorylation-related genes, antizyme inhibitor of ornithine decarboxylase, protein phosphatase-1beta, 35-kDa peroxisomal membrane protein, and cystic fibrosis transmembrane conductance receptor were highly expressed in tumor tissue, whereas pepsinogen A, Na-K ATPase alpha subunit, nerve growth factor receptor, and alpha-tropomyosin were highly expressed in normal tissue. In addition, 3 unknown genes were found to be differentially expressed in paired gastric tissues. These differentially expressed genes may provide significant opportunities for further understanding of gastric carcinogenesis and the molecular diagnosis of gastric cancer.
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PMID:Identification of differentially expressed genes in normal and tumor human gastric tissue. 1105 45

Extracellular signal-regulated protein kinases (ERKs) are important in many cellular functions. We and others have previously reported that prolonged exposure of gastric parietal cells to epidermal growth factor (EGF) enhanced gastric acid secretion stimulated by secretagogues via ERKs. In this study, we examined whether ERKs regulated H(+),K(+)-ATPase alpha-subunit gene expression using a gastric cancer cell line, AGS. EGF induced ERK activity time- and dose-dependently with a maximal effect observed at 10 min and 10 nM, respectively. The MEK inhibitors, U0126 and PD-98059, dose-dependently inhibited the ERK activity stimulated by EGF. To test H(+),K(+)-ATPase alpha-subunit gene expression, we transfected AGS cells with a plasmid containing a canine H(+),K(+)-ATPase alpha-subunit gene promoter fused to a luciferase reporter gene. EGF induced luciferase activity in transfected cells; this effect was inhibited by the MEK inhibitors, suggesting that EGF-induced gene expression involved the ERK pathway. When AGS cells were transfected with the reporter plasmids in conjunction with an expression vector encoding constitutively active MEK1, luciferase activity was strongly enhanced; this effect was attenuated by the MEK inhibitors or by an additional cotransfection of dominant negative MEK1. Taken together, our results led us to conclude that the ERK pathway may mediate H(+),K(+)-ATPase alpha-subunit gene expression, contributing to gastric acid secretion in parietal cells.
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PMID:Extracellular signal-regulated protein kinases mediate H(+),K(+)-ATPase alpha-subunit gene expression. 1181 3

To identify genes whose alterations lead to gastric cancer, gene expression profiles have been obtained from 22 gastric cancer tissues and their surrounding gastric mucosa tissues. A total of 16 genes were differentially expressed in more than 50% of gastric cancer tissues compared with surrounding gastric mucosa tissues. Genes such as HMG-Y, fibroblast collagenase inhibitor, and osteopontin are among those that are overexpressed in over 50% of the gastric cancer tissues. Dihydrodiol dehydrogenase, ribonuclease A, and glutathione peroxidase are among those genes that are underexpressed in over 50% of the gastric cancer tissues. We identified genes that are associated with clinical phenotypes of patients with gastric cancers. Alpha-II spectrin, Na/K-ATPase and KIAA0111 are those that are enhanced in intestinal type of gastric cancer. Gene such as platelet-endothelial tetraspan antigen 3 was enhanced in highly metastatic gastric cancer tissues.
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PMID:Identification of genes differentially expressed between gastric cancers and normal gastric mucosa with cDNA microarrays. 1212 92

After incubation with 2-butylamino-2-demethoxy-hypocrellin A (2-BA-2-DMHA), photodynamically induced change in the cytoplasmic free calcium concentration ([Ca(2+)](i)) and its effect on cell damage were investigated in human gastric cancer (MGC-803). Fluorescence spectrophotometry measurement indicated that the photosensitization of MGC-803 by 2-BA-2-DMHA caused an increase in intracellular calcium [Ca(2+)](i), and this increase in [Ca(2+)](i) showed a dependence on the concentration of 2-BA-2-DMHA, light dose and extracellular [Ca(2+)](e). This phenomenon of intracellular calcium accumulation was further confirmed by using laser scanning confocal microscopy (LSCM). Furthermore, the results from MTT assay and flow cytometry analysis suggested that chelation of extracellular calcium by EGTA or intracellular calcium by BAPTA could inhibit photodynamically induced cell killing, while increase of [Ca(2+)](i) by thapsigargin (TG), a highly specific inhibitor of the Ca(2+)-ATPase, or by A23187, a calcium ionophore could enhance this action. Meanwhile, the nucleus morphology was also investigated by fluorescence microscopy. The results indicated that the increase in intracellular Ca(2+) concentration was responsible for 2-BA-2-DMHA photodynamically induced damage to MGC-803.
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PMID:Role of calcium in phototoxicity of 2-butylamino-2-demethoxy-hypocrellin A to human gastric cancer MGC-803 cells. 1258 63


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