Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The human hepatoma cell line Hep G2 was used to investigate amino acid transport systems in human liver tissue. The ubiquitous transport systems responsible for the uptake of most neutral amino acids (systems A, ASC and L) were found to be present. Transport system A was predominant for proline uptake but system ASC was the major Na(+)-dependent transport system, particularly for glutamine. The specific hepatic system N was functional, but only partially mediated glutamine uptake. The study of Na(+)-independent arginine uptake demonstrated the presence of the cationic transport system Y+, reflecting the transformed nature of Hep G2 cells.
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PMID:Amino acid transport systems in the human hepatoma cell line Hep G2. 133 97

Anti-HD antibody was not detected in 342 patients with acute type B hepatitis including 8 patients with fulminant hepatitis. Anti-HD antibody was detected in 10 out of 1668 HBV carriers. The overall prevalence was 0.59 percent. Two (0.34%) out of 586 ASC, 3 (0.43%) out of 690 patients with CH and 5 (1.47%) out of 338 patients with LC were positive for anti-HD antibody. No anti-HD antibody was detected in sera of 54 patients with HCC. The prevalence of anti-HD antibody was relatively high in patients with LC, however, HDV infection was relatively rare in Japan and it does not always play a major role in progression of liver disease. The prevalence of HDV infection in HBV carriers has not changed in Japan during the last ten years (1.3% vs. 1.49%).
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PMID:Epidemiology of HDV infection in Japan. 202 Jul 25

The Na(+)-dependent transport of L-alanine into plasma membrane vesicles from Yoshida ascites hepatoma (AH-130) cells in the exponential and stationary phase of growth has been studied. A transient accumulation of the amino acid occurred in the presence of an inwardly directed sodium gradient, in both conditions. However, the height and the shape of the overshoot curve differed noticeably in the two preparations. The accumulation ratio increased three-fold and the maximal uptake value occurred at an earlier time in plasma membrane vesicles from exponential growing rather than stationary phase cells. This might suggest that one of the two systems, A or ASC, serving hepatocytes, is fully expressed only in the exponential phase of growth or, alternatively, that the kinetic parameters of a possibly unique transport system are modified. Inhibition, countertransport as well as adaptive stimulation experiments and kinetic studies suggested the presence of a unique carrier-mediated transport of alanine in both phases of growth. The Vmax value was drastically reduced in the stationary phase of growth whereas the Km value was almost the same in both preparations. Therefore, the differences in time courses observed could be related to changes of the Vmax of a single transport agency rather than to the appearance/disappearance of an additional transport system (e.g. system A) in the conditions studied.
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PMID:Alanine transport in plasma membrane vesicles from Yoshida ascites hepatoma cells (AH 130) in the exponential and stationary phase of growth. 208 37

IL2R+ Leu11+ cells (A) and HLADR+ Leu11+ cells (B) of peripheral blood in patients with various liver diseases and ASCs were measured using double colour immunofluorescence assay of MoAb with FACS flow cytometry. 1) The mean % of IL2R+ Leu11+ cells which was 0.5 +/- 0.2 in healthy controls, decreased significantly in HCC in comparison with CALD, ASC and healthy controls, and in ASC rather than in healthy controls. They (A) were less than 0.1% in eight of thirteen cases with HCC, in one of twenty cases with CALD and of eleven ASCs, respectively. 2) In the mean % of HLADR+ Leu11+ cells which was 2.9 +/- 1.8 in healthy controls there was not a significant difference among HCC, CALD, ASC, AH and healthy controls. They (B) were less than 0.1% only in one case with HCC. 3) The value of fluorescence intensity of IL2R on IL2R+ Leu11+ cells reduced in B-CALD, ASC, AH and HCC, and one of HLADR on HLADR+ Leu11+ cells increased in CALD. These results suggested that the decrease of IL2R+ Leu11+ cells was due to the existence of HCC.
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PMID:[Circulating mature NK (Leu11+) cells positive for IL2 receptor and HLA-DR in patients with various liver diseases and asymptomatic HBsAg carriers]. 256 Apr 87

Substrate regulation of System A transport activity in rat H4 hepatoma cells is described. The uptake of several amino acids was tested in the presence of system-specific inhibitors. System A activity was increased in a RNA- and protein synthesis-dependent manner by amino acid deprivation of the cells (adaptive regulation), whereas transport by Systems ASC, N, y+, and L was unaffected. Unlike human fibroblasts, the H4 cells did not require serum to exhibit the depression of System A. At cell densities between 88 X 10(3) and 180 X 10(3) cells/cm2, the degree of adaptive regulation was inversely related to cell density. Both transport of AIB and adaptive regulation of System A were nearly abolished if either K+ or Li+ was substituted for Na+ in the medium. The presence of cycloheximide or tunicamycin blocked further increases in starvation-induced activity within 1 hr of addition, suggesting the involvement of a plasma membrane glycoprotein. In contrast, if the medium was supplemented with actinomycin after the stimulation of System A had begun, the activity continued to increase for an additional 2 hr before being slowed by the inhibitor. The contributions of trans-inhibition and repression to the amino acid-induced decay of System A activity were estimated for several representative amino acids. In general, the System A activity in normal rat hepatocytes was much less sensitive to trans-inhibition than the corresponding activity in H4 hepatoma cells. The half-life values for the amino acid-dependent decay of System A ranged from 0.5 to 2.0 hr.
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PMID:Adaptive regulation of neutral amino acid transport System A in rat H4 hepatoma cells. 257 76

the transport of amino acids by both normal rat hepatocytes and rat H4 hepatoma cells has been tested for inactivation by sulfhydryl-preferring, protein-modifying reagents. Amino acid transport by systems A, ASC, N, L, and y+ in the H4 hepatoma cells was relatively resistant to inactivation by the alkylating reagent N-ethylmaleimide (NEM), whereas uptake mediated by systems A, ASC, and L was decreased in normal rat hepatocytes. In contrast, nearly all of the amino acid transport systems in both cell types were inhibited strongly by p-chloromercuribenzene sulfonate (PCMBS). The exceptions were the H4 hepatoma system y+ activity (72% of control) and system L-mediated uptake (121% of control) in normal hepatocytes. Although transport via system A was equally sensitive to inhibition by PCMBS in both cell types, substrate-dependent protection from this inactivation was observed only in the H4 hepatoma cells. These results illustrate the significant differences that exist between normal and transformed liver cells in respect to amino acid transport inactivation by sulfhydryl reagents.
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PMID:Inactivation of amino acid transport in rat hepatocytes and hepatoma cells by PCMBS. 284 94

The transport of L-threonine and L-glutamine into murine P388 leukemia cells has been characterized. Threonine appears to be a specific substrate for a Na+-dependent amino acid transport system similar to system ASC of the HTC hepatoma cell. Threonine transport is uninhibited by 2-aminobicyclo[2,2,1]heptane-2-carboxylic acid and alpha-(methylamino)isobutyric acid, shows a pattern of transport similar to that seen in HTC hepatoma cells over the pH range of 5.5-7.5, and is inhibited by L-serine and L-cysteine. Approximately two-thirds of glutamine transport into P388 cells also appears to enter P388 cells via this ASC-analogous system. However, based upon (a) inhibition studies with threonine (where the K1 of threonine inhibition of glutamine transport was 7-fold the Km of threonine transport), (b) inhibition analysis of glutamine transport with various amino acids and amino acid analogues, and (c) different patterns of transport between threonine and glutamine over the pH range of 5.5-7.5, approximately one-third of glutamine transport can be attributed to a second Na+-dependent amino acid transport system. This system appears to be similar to the system N of rat hepatocytes. Glutamine and threonine do not appear to enter P388 cells via systems A or L to any significant degree. P388 cells do not appear to exhibit 'adaptive regulation' of amino acid transport. Differences in 'adaptive regulation' could therefore not be utilized for comparing threonine and glutamine transport.
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PMID:Characterization of L-threonine and L-glutamine transport in murine P388 leukemia cells in vitro. Presence of an N-like amino acid transport system. 308 65

The transport of glycine and L-lysine into murine P388 leukemia cells has been examined. Glycine transport appears to be shared by both systems A and ASC in P388 cells. Glycine transport is Na+-dependent and is effectively blocked by alpha-(methylamino)isobutyric acid, threonine and alanine but only a marginal reduction in transport is seen with 100-fold excess cold 2-aminobicyclo[2,2,1]heptane-2-carboxylic acid. System gly is not expressed in P388 cells. Lysine is largely transported by a Na+-independent, pH-insensitive system with a Km of 0.079 mM. Lysine transport is relatively unaffected by the addition of 100-fold excess cold alpha-(methylamino)isobutyric acid, 2-aminobicyclo[2,2,1]heptane-2-carboxylic acid and the anionic amino acids, L-glutamate and L-aspartate. A partial inhibition of lysine transport was observed with L-threonine and L-leucine while L-arginine and L-histidine radically decreased lysine transport. Lysine appears to be transported by a system similar to the system y+ seen in cultured human fibroblasts, Ehrlich ascites cells, and hepatoma cell lines.
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PMID:Further studies on amino acid transport in murine P388 leukemia cells in vitro. Presence of system y+. 310 85

1. The occurrence and characterization of acidic amino acid transport in the plasma membrane of a variety of cells and tissues of a number of organisms is reviewed. 2. Several cell types, especially in brain, possess both high- and low-affinity transport systems for acidic amino acids. 3. High-affinity systems in brain may function to remove neurotransmitter amino acid from the extracellular environment. 4. Many cell systems for acidic amino acid transport are energized by an inwardly directed Na+ gradient. Moreover, certain cell types, such as rat brain neurons, human placental trophoblast and rabbit and rat kidney cortex epithelium, respond to an outwardly directed K+ gradient as an additional source of energization. This simultaneous action may account for the high accumulation ratios seen with acidic amino acids. 5. Rabbit kidney has been found to have a glutamate-H+ co-transport system which is subject to stimulation by protons in the medium. 6. Acidic amino acid transport in rat brain neurons occurs with a stoichiometric coupling of 1 mol of amino acid to 2 mol of Na+. For rabbit intestine, one Na+ is predicted to migrate for each mol of amino acid. 7. Uptake in rat kidney cortex and in high-K+ dog erythrocytes is electrogenic. However, uptake in rabbit and newt kidney and in rat and rabbit intestine is electroneutral. 8. Na+-independent acidic amino acid transport systems have been described in the mouse lymphocyte, the human fibroblast, the mouse Ehrlich cell and in rat hepatoma cells. 9. In a number of cell systems, D-acidic amino acids have substantial affinity for transport; D-glutamate, in a number of systems, however, appears to have little reactivity. 10. Acidic amino acid transport in some cell systems appears to occur via the "classical" routes (Christensen, Adv. Enzymol. Relat. Areas Mol. Biol. 49, 41-101, 1979). For example, uptake in the Ehrlich cell is partitioned between the Na+-dependent A system (which transports a wide spectrum of neutral amino acids), the Na+-dependent ASC system (which transports alanine, serine, threonine, homoserine, etc.), and the Na+-independent L system (which shows reactivity centering around neutral amino acids such as leucine and phenylalanine). Also, a minor component of uptake in mouse lymphocytes occurs by a route resembling the A system. 11. Human fibroblasts possess a Na+-independent adaptive transport system for cystine and glutamate that is enhanced in activity by cystine starvation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acidic amino acid transport in animal cells and tissues. 330 25

A number of amino acids, most noticeably asparagine, were capable of inducing ornithine decarboxylase in H-35 rat hepatoma cells. The effective amino acids were all neutral and were substrates of the Na+-dependent transport systems A, ASC and N. Transport inhibitor studies indicated that there was an excellent correlation between the level of enzyme activity induced and the initial rate of asparagine transport into the cells by the A and the N systems. It is proposed that the activation of the Na+-dependent, pH-sensitive amino acid transport systems and the subsequent intracellular pH and ionic perturbation constitute part of the initiation signals for cell activation.
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PMID:Asparagine transport and the induction of ornithine decarboxylase in H-35 rat hepatoma cells. 345 89


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