Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transgenic mice bearing the elastase I promoter--SV40 T-antigen fusion gene (ELSV) develop pancreatic acinar cell carcinomas by 3 to 6 months of age. The purpose of the study was to determine if pancreatic carcinomas and dysplastic pancreas from the Tg (Ela-1, SV40E + Ela-1, neo) Bri19 strain of ELSV transgenic mice express gastrin (CCK-B) receptors. To accomplish this, we utilized iodine 125 (125I)-gastrin binding studies, reverse transcription-polymerase chain reaction (RT-PCR), and Southern blot analysis to examine pancreatic carcinomas from 26-week-old male ELSV transgenic mice, dysplastic pancreas from 8-week-old male ELSV transgenic mice, and normal pancreas from 30-week-old nontransgenic male mice (SJL/J) and from 8-week-old nontransgenic male mice (B6SJLF1/J). No saturable gastrin binding to normal nontransgenic mouse pancreas was found. In contrast, saturable gastrin binding was detected at pH 6.5, 22 degrees C, in 9 of 13 pancreatic carcinomas and all 5 dysplastic pancreata. Competitive inhibition 125I-gastrin binding assays showed gastrin bound to a single class of high-affinity receptors (receptor binding affinity [Kd] 0.11 +/- 0.02 nM, binding capacities ranging from 1 to 60 fmol/mg protein for pancreatic carcinomas; Kd: 0.15 +/- 0.04 nM, binding capacities ranging from 1 to 9 fmol/mg protein for dysplastic pancreas). RT-PCR and Southern blot analysis confirmed 125I-gastrin binding studies by demonstrating gastrin (CCK-B) receptor mRNA expression in pancreatic carcinomas and dysplastic pancreas but an absence of mRNA expression in normal nontransgenic mouse pancreas. In conclusion, pancreatic carcinomas and dysplastic pancreas in ELSV transgenic mice novelly express gastrin (CCK-B) receptors. This expression may provide a growth advantage to acinar cells as part of the multistage process of carcinogenesis.
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PMID:Novel expression of gastrin (CCK-B) receptors in pancreatic carcinomas and dysplastic pancreas from transgenic mice. 831 Nov 22

To investigate the cellular mechanisms of ovarian epithelial carcinogenesis, a series of progressively transformed rat ovarian surface epithelial (ROSE) cell lines were developed and studied. Transfection of primary ROSE cells and an immortalized ROSE line (ROSE 199) with the pSV3neo plasmid (SV40 T-antigen) yielded transformed lines which retained epithelial morphology. In vivo selection of these pSV3neo cell populations resulted in further phenotypic transformation. Transfection of ROSE 199 with pSV2neo/c-H-rasEJ (rasEJp21) resulted in a malignant line which appeared fibroblast-like and formed invasive sarcomas both in athymic mice and in immunocompetent rats. Gap junctional intercellular communication (GJIC) and cell-cell adhesion were studied in this series of ROSE lines. Both c-H-rasEJ-transformation and in vivo selection resulted in a significant reduction of GJIC between adjoining cells and a transition of in vitro migration as continuous epithelial sheets to the dissociation of individual cells. This apparent shift in cell adhesiveness was associated with reduced expression of the E-cadherin adhesion molecule. Our data suggest that neoplastic progression of the ovarian surface epithelium may be associated with concomitant reductions in GJIC, E-cadherin expression and functional adhesiveness.
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PMID:An in vitro model of ovarian epithelial carcinogenesis: changes in cell-cell communication and adhesion occurring during neoplastic progression. 832 8

To test the hypothesis that a mutator phenotype may be associated with carcinogenesis (L. A. Loeb, Cancer Res., 51: 3074-3079, 1991), we have compared the fidelity of double-stranded DNA replication and the efficiency of mismatch repair in extracts from normal diploid and malignantly transformed human cells. Included was a diploid fibroblast strain and its transformed derivative, as well as a second diploid fibroblast strain and HeLa cells. The fidelity of DNA replication by cytoplasmic extracts in the presence of simian virus 40 large tumor antigen (SV40 T-antigen) was measured using a forward mutagenesis assay. The replicated DNA consisted of double-stranded M13 mp2 DNA containing the SV40 origin of replication and the lacZ alpha complementation gene as a target sequence for scoring mutations. T-antigen-dependent replication was detected in all cell extracts, with those from transformed cells having the greatest activity. No differences in replication fidelity were detected between normal and transformed cell extracts. Using a heteroduplex containing a G.G mispair, we also detected mismatch repair activity in the cell extracts, including efficient repair in extracts from malignantly transformed cells. While these data do not eliminate the possibility that a mutator phenotype may be associated with carcinogenesis, they do suggest that genetic instability associated with transformation does not involve reduced fidelity of replication of undamaged DNA or reduced mismatch repair efficiency.
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PMID:Fidelity of DNA replication by extracts of normal and malignantly transformed human cells. 839 21

The effects of prolonged administration of the diuretic amiloride on pancreatic carcinogenesis induced by azaserine and on the labeling index of carcinogen-induced pancreatic lesions were investigated in Wistar rats. Rats were given 25 weekly injections of 10 mg/kg body weight azaserine and also 5 mg/kg body weight amiloride every other day until the end of the experiment at week 62. Carcinogen-induced pancreatic lesions were examined by histochemical techniques and were classified as ATPase-positive or ATPase-negative. In week 62, quantitative histologic analysis showed that prolonged administration of amiloride significantly reduced the number and size (as percent of parenchyma) of ATPase-positive pancreatic lesions, which are closely correlated with the subsequent development of pancreatic cancer. Amiloride also significantly decreased the labeling index of carcinogen-induced pancreatic lesions, but not of the surrounding acinar cells. In contrast, amiloride has no significant influence on the number and size of ATPase-negative pancreatic lesions. These findings indicate that amiloride inhibits pancreatic carcinogenesis, and that this effect may be related to the reduction of ATPase-positive lesions and to amiloride's inhibition of cell proliferation in neoplastic lesions of the pancreas.
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PMID:Inhibition by amiloride of experimental carcinogenesis induced by azaserine in rat pancreas. 882 43

Radiation-induced carcinogenesis of the rat liver using iridium-192 seeds as an intrahepatic radioactive source was studied by enzyme histochemical means. Rats were divided into six groups according to various combinations of one or two iridium-192 or stainless steel seeds and whether they were given a diet containing 0.05% phenobarbital (PB) or a basal diet (BD). Each group were sacrificed at 20, 40, and 60 weeks after intrahepatic insertion of the iridium-192 or stainless steel seeds. gamma-Glutamyl transpeptidase (GGT), glucose-6-phosphatase (G6Pase), and adenosine triphosphatase (ATPase) were stained in the liver tissues, and GGT-positive foci were quantified. Liver neoplasm was not evident, but enzyme-altered foci (EAF) were induced by gamma-ray irradiation. At every point (20, 40, and 60 weeks) after the insertion of the seeds, the GGT-positive area was larger in the rats given than those given BD. Moreover, despite the iridium-192 radioactivity decay, EAF developed continuously in the rats given PB, and persisted in those given BD from 40 to 60 weeks after insertion. These results indicated that phenobarbital promotes the development of EAF initiated by irradiation, as it promotes the process of chemical carcinogenesis in the rat liver.
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PMID:Promoting effects of phenobarbital on the enzyme-altered foci induced by intrahepatic gamma-ray-irradiation in the rat liver. 884 57

In an attempt to seek out new factors that are related to colorectal carcinogenesis at the molecular level, subtractive hybridization between cDNA of normal mucosal tissues and mRNA of colorectal carcinoma tissues was performed. Subsequent screenings of the cDNA libraries, constructed from normal mucosal tissues, using the "subtractive probes" generated a total of 46 clones that were expressed in normal mucosa but were either expressed at a significantly reduced level or not expressed at all in cancer tissues. Partial nucleotide sequences of all of these cDNA clones were determined, and sequence homology analyses were performed with the Genbank database. Of the 46 cDNA samples, 44 contained substantial sequence homologies with 32 immunoglobulin gene fragments, a helix-loop-helix basic phosphoprotein gene, an acidic ribosomal phosphoprotein P2 gene, a BLR1 gene for Burkitt's lymphoma receptor 1 gene, D5S419 DNA segment containing (C-A) repeats, a glucokinase (GCK) gene, a Na+, K+-ATPase alpha-subunit gene, a histocompatibility system HLA-DR heavy-chain gene, a dystrophic gene, a mucin (MUC2) gene, a mu-glutathione S-transferase gene, a Menkes disease protein gene, and a 40-kDa keratin intermediate filament precursor gene. The remaining two cDNA clones (now registered under GenBank accession numbers U17714 and U20428) showed few (less than 60%) sequence homologies with any known sequences in the GenBank database and, therefore, may represent novel genes whose expression was down-regulated in human colorectal carcinomas. The possible clinical significance of these findings and the involvement of these two genes in the carcinogenesis of colorectal as well as other cancers are being investigated.
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PMID:Characterization of colorectal-cancer-related cDNA clones obtained by subtractive hybridization screening. 929 8

We have performed differential display comparing gene expression from cell lines derived from human colorectal tumors. The cell lines were selected for study based on their ability to form metastases following injection into athymic mice. One gene which was expressed exclusively by the metastatic lines was identified as human acylphosphatase (e.c. 3.6.1.7, acylphosphate phosphohydrolase). The expression of this gene was confirmed by RT-PCR using gene-specific primers. This gene product catalyzes the hydrolysis of phosphorylated intermediates of Na+/K(+)-ATPase and of Ca(2+)-ATPases of mammalian cells. Changes in the activity of the Na+/K(+)-ATPase pump, regulated by acylphosphatase, have been previously reported in chemically-induced colonic tumors. The differential expression of this gene in the human metastatic colorectal lines suggests it may be involved in the metastatic phenotype.
Carcinogenesis 1997 Dec
PMID:The expression of acylphosphatase is associated with the metastatic phenotype in human colorectal tumors. 945 Apr 95

The effects of galanin on pancreatic carcinogenesis induced by azaserine and on the norepinephrine concentration in the pancreas were investigated in male Wistar rats. Rats were given weekly injections of 10 mg/kg body weight of azaserine for 25 weeks and 8 microg/kg body weight of galanin in depot form every other day for 62 weeks. Azaserine-induced pancreatic lesions were examined with hematoxylin and eosin and histochemical techniques. In week 62, quantitative histological examination showed that prolonged administration of galanin significantly reduced the number and size (as percent of parenchyma) of adenosine triphosphatase-positive pancreatic lesions, which are correlated closely with the ultimate development of pancreatic cancer. The number of pancreatic adenocarcinomas in rats treated with galanin was significantly less than in controls. Galanin also significantly decreased the bromodeoxyuridine-labeling index of azaserine-induced pancreatic lesions and the norepinephrine concentration in the pancreas. Our findings indicate that galanin inhibits pancreatic carcinogenesis and that such inhibition may be related to the suppression of sympathetic nervous system activity and subsequently to the inhibition of cell proliferation in neoplastic lesions of the pancreas.
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PMID:Inhibition by galanin of experimental carcinogenesis induced by azaserine in rat pancreas. 945

Deoxyribonucleic acid (DNA) oncoviruses can induce neoplastic transformation by interfering with proliferative proteins. Simian virus 40 (SV40) has been shown to induce brain tumors, osteosarcoma, lymphoid tumors and malignant mesothelioma in hamsters and SV40-like DNA sequences corresponding to the Rb-pocket binding domain of SV40 T-antigen (Tag) have been detected in the same human tumors. Since only a small percentage of people exposed to asbestos fibers develop a malignant mesothelioma, SV40 has been suspected to co-operate with the fibers in the neoplastic transformation or even to itself induce the onset of malignant mesothelioma in patients without expositive history. The mechanism that seems to be involved in the SV40-induced carcinogenesis process is mediated by interaction of Tag, both with p53 and Rb proteins, leading to their functional inactivation that is responsible for the removal of their inhibitory cell cycle effect which determines the increase of the number of cells entering the G1-S phase. Up to now the source of SV40 human infections has not yet been completely identified even though administration from 1957-1965 of SV40 contaminated polio vaccines is highly suspected. Horizontal infection by sexual transmission has been also hypothesized. Due to the important public health implications further investigations are required in order to establish both the source and the carcinogenetic role of simian virus 40 in humans.
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PMID:Simian virus 40 and human cancer. 968 9

Reactive oxygen species (ROS) and reactive metabolic intermediates generated from various chemical carcinogens are known to play an important role in cell damage and in the initiation and progression of carcinogenesis. Many radical scavengers, interestingly naturally occuring antioxidants have been found to be effective in inhibiting the induction of carcinogenesis by a wide variety of chemical carcinogens. Studies have also indicated that various spice principles form an important group as antioxidants. In the present study our goal was to investigate whether piperine an pungent principle of black and long peppers was able to inhibit or reduce the oxidative changes induced by chemical carcinogens in rat intestinal model. Carcinogenesis was initiated in intestinal lumen of male rats with 7,12,dimethyl benzanthracene, dimethyl amino-methyl azobenzene and 3-methyl cholenthrene. Oxidative alterations were assessed by determining thiobarbituric reactive substances, mainly malonaldehyde (as a measure of lipid peroxidation), thiol status and expression of gamma-GT and Na+-K+-ATPase activity in intestinal mucosa. Data indicated that carcinogens treatment induced GSH depletion with substantial increase in thiobarbituric reactive substances and enzyme activities. Piperine treatment with carcinogens resulted in inhibition of thiobarbituric reactive substances. It mediated a significant increase in the GSH levels and restoration in gamma-GT and Na+-K+-ATPase activity. The studies thus indicate a protective role of piperine against the oxidative alterations by carcinogens. It may be suggested that piperine modulates the oxidative changes by inhibiting lipid peroxidation and mediating enhanced synthesis or transport of GSH thereby replenishing thiol redox.
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PMID:Piperine modulation of carcinogen induced oxidative stress in intestinal mucosa. 987 61


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