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 effects of phorbol ester on cell growth inhibition by transforming growth factor beta 1 (TGF-beta 1) in human hepatoma cell lines, Mahlavu and PLC/PRF/5, were investigated. TGF-beta 1 (2.5 to 10 pM) alone could not inhibit the growth of Mahlavu cells, whereas in the presence of 12-O-tetradecanoyl phorbol 13-acetate (TPA) at 1 ng/ml, TGF-beta 1 could suppress their growth in a dose-dependent manner. The growth of PLC/PRF/5 cells could be inhibited by addition of TGF-beta 1 (2.5 to 10 pM) alone in a dose-dependent manner, and this action was not affected by TPA (1 ng/ml). The TGF-beta 1 inhibition induced by TPA in Mahlavu cells could not be cancelled by addition of protein kinase C inhibitor, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H7) (10 microM) or staurosporin (1 nM). Thus, TPA could induce TGF-beta 1 inhibition of cell growth in Mahlavu cells which did not respond to TGF-beta 1 alone, and activation of protein kinase C does not seem to be behind this TPA action.
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PMID:Effects of phorbol ester on cell growth inhibition by transforming growth factor beta 1 in human hepatoma cell lines. 216 81

More than 90% of lipids of hepatitis B virus surface antigen (HBsAg) particles produced by two human hepatoma cell lines (huGK-14 and PLC/PRF/5) were composed of phospholipids, with phosphatidylcholine being the dominant component, accounting for more than 80% of total membrane lipids. Analysis of subclass compositions of phospholipids of HBsAg particles and the host cell lines revealed that 1,2-diacyl glycerophosphocholine was preferentially incorporated into the membrane of the HBsAg particles, although both host cell lines contained extremely high concentrations (more than 60% of total phospholipids) of ether-linked phospholipids. Phospholipids of other hepatoma cell lines (HuH-7, Hep-G2, and huL-1) which were not associated with hepatitis B virus (HBV) infection, were composed mostly of 1,2-diacylglycerophospholipids. Activities of dihydroxyacetone-phosphate acyltransferase, which is known to be an obligatory enzyme in ether lipid biosynthesis, were found to be elevated by three- to fourfold in both huGK-14 and PLC/PRF/5 cells compared to those of other hepatoma cell lines. The results suggest a possible relationship between HBV-induced hepatocellular carcinogenesis and the drastic change in the metabolism of membrane phospholipids.
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PMID:Lipid composition of hepatitis B virus surface antigen particles and the particle-producing human hepatoma cell lines. 216 17

Transforming growth factor-beta (TGF-beta) modified production of the major human acute phase reactant, C-reactive protein (CRP), induced by the inflammatory cytokines, IL-1 beta or IL-6. CRP mRNA accumulation in the hepatoma PLC/PRF/5 cell line was slightly more rapid, but of smaller magnitude in response to IL-1 beta (fourfold increase) than to IL-6 (10-fold increase); however, the amount of CRP protein accumulating in the culture medium was similar for both cytokines. TGF-beta at concentrations greater than or equal to 0.1 pg/ml inhibited the induced IL-1 or IL-6 CRP production; whereas concentrations less than 0.1 pg/ml slightly enhanced CRP synthesis. Addition of TGF-beta to the cultures up to 16 h after the PLC/PRF/5 cells were already exposed to IL-1 or IL-6 resulted in the cessation of CRP production. CRP mRNA accumulated in hepatoma cells treated with both TGF-beta and IL-6, although CRP protein synthesis was inhibited. A similar pattern of inhibition of CRP production by TGF-beta occurred when Hep 3B.2 cells were treated with a mixture of IL-1 and IL-6. Enhanced production of CRP was observed only when TGF-beta was added to the cells before the cytokine. This enhanced CRP response was sensitive to cycloheximide. TGF-beta added along with IL-6 inhibited the metabolic labeling of CRP with [35S]methionine; however, enhanced incorporation of [35S]methionine into CRP was observed when the cells were exposed to TGF-beta before IL-6 addition. Therefore, TGF-beta is potentially a potent regulator of CRP synthesis by hepatocytes at the post-transcriptional level.
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PMID:Regulation of cytokine-induced human C-reactive protein production by transforming growth factor-beta. 217 May 18

Adenoviruses, types 2 and 12 induce amplification of SV40 DNA sequences in cells of the SV40-transformed human newborn kidney cell line, NB-E. Similarly, integrated hepatitis B virus DNA sequences in the human hepatoma cell line, PLC/*PRF/5, and bovine papillomavirus (BPV) DNA sequences in BPV-transformed mouse cells (ID13) are amplified by adenovirus infection. Thus, similar to herpes group or vaccinia viruses or DNA damaging agents, adenoviruses are able to mediate selective DNA amplification in addition to their reported mutagenic and chromosome damaging effects. The role of amplification of integrated viral DNA sequences in development and progression of specific tumors (e.g. hepatocellular carcinoma) remains to be determined.
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PMID:Adenovirus infection induces amplification of persistent viral DNA sequences (simian virus 40, hepatitis B virus, bovine papillomavirus) in human and rodent cells. 217 Dec 40

A transient depression of HBV serologic markers has been reported for some chronically infected patients treated with human interferons. To determine a molecular basis for these observations, a human, HBV-carrying, hepatocellular carcinoma cell line (PLC/PRF/5) was treated with human alpha, beta, or gamma interferons. Administration of these interferons resulted in a marked depression of HBV surface antigen (HG-sAg) levels in the culture medium. This inhibition was transient, with media levels of HBsAg rising substantially within 48 hours following the termination of interferon treatment. Cell growth rates were not affected by alpha interferon treatment, indicating that overall cell protein synthesis was not substantially altered. Although all three classes of interferons were effective in lowering HBsAg levels in the culture medium, intracellular levels of HBsAg-specific RNA were unaffected. These results suggest that the transient depression of HBV serologic markers in interferon-treated patients may be a consequence of the failure to disrupt the intracellular pools of HBV RNA in the liver.
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PMID:Direct modulation of HBV surface antigen in a human, HBsAg-producing hepatocellular carcinoma cell line by alpha, beta, or gamma interferons. 217 72

We have identified a tumour-related 43 kd cytoplasmic protein (LC/p43) using a monoclonal antibody against the total proteins of human hepatoma cell line PLC/PRF/5. LC/p43 is preferentially expressed in a variety of tumours of human and animal origin, whereas no expression was detected in several normal adult tissues tested. LC/p43 expression was induced in rodent fibroblasts upon transfection with several viral oncogenes. Expression in non-transformed peripheral blood lymphocytes could be induced by treatment with phytohaemagglutinin (PHA) and subsequent culture with interleukin II, whereas retinoic acid treatment of transformed cells caused a drastic reduction of the antigen in the cells. Sequence analysis of three tryptic peptides of LC/p43 revealed 50-70% homology to different domains of the eukaryotic and prokaryotic translation-elongation factors EF1-alpha and EF-Tu, respectively.
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PMID:Tumour-related expression of a translation-elongation factor-like protein. 219 92

The in vitro interaction of mercury, copper (II) and cadmium with human glutathione transferase (GST) pi was studied using reduced glutathione (GSH) and 1-chloro-2,4-dinitrobenzene as substrate. Tumor specific human GST pi was isolated from the human hepatoma derived PLC/PRF/5 cell line. The inhibition of the GST pi activity was dose dependent. Kinetic studies never revealed competitive inhibition. A parabolic inhibition was found with GSH as the variable substrate. The heavy metals are spontaneously conjugated with GSH and cysteine, but interact with GST pi by direct binding to this protein. This binding could have a protective function against heavy metals.
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PMID:In vitro interaction of mercury, copper (II) and cadmium with human glutathione transferase pi. 221 73

The S-gene fragments of hepatitis B virus (HBV) DNA in serum, or integrated in chromosomes of human hepatoma cells (PLC/PRF/5), were amplified by the polymerase chain reaction, cloned into an M13 phage vector, and then sequenced only for adenine. The subtype determinant d or y was established by the presence or absence of adenine as nucleotide 365, and w or r by that of nucleotide 479 in the S gene. The results were identical with those obtained by enzyme immunoassay with monoclonal antibodies. A high sensitivity for the detection of HBV DNA, amplified by the polymerase chain reaction, allowed subtyping of HBV in sera containing HBsAg in concentrations too low to be subtyped by immunological methods. Furthermore, subtyping at the nucleotide level can be applied to tissues containing HBV DNA sequences in integrated forms, such as hepatocellular carcinomas, stored frozen or in formalin.
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PMID:Subtyping hepatitis B virus DNA in free or integrated forms by amplification of the S-gene sequences by the polymerase chain reaction and single-track sequencing for adenine. 237 Feb 86

The in vitro effects of alpha-difluoromethyl ornithine (DFMO) on the growth and the secretion of alpha-fetoprotein (AFP) and albumin in human hepatoma cell line PLC/PRF/5 were studied. DFMO caused a marked reduction in the growth rate and de novo synthesis of DNA, whereas secretion of AFP and albumin was not altered. These data indicate that AFP and albumin secretion are neither linked to polyamine synthesis nor to cellular proliferation in human hepatoma cells.
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PMID:Effects of alpha-difluoromethyl ornithine on alpha-fetoprotein and albumin secretion in human hepatoma cell line, PLC/PRF/5. 241 87

Hepatitis B virus (HBV) gene expression was investigated in the PLC/PRF/5 human hepatoma cell line and the mouse L-cell line transfected with HBV DNA by modulating the in vitro growth conditions. Both cell lines contain the viral genome integrated into cell chromosomes and both have been shown to produce hepatitis B surface antigen only. Treatment with 5-azacytidine (5-azaC) did not enhance hepatitis B core antigen (HBcAg) synthesis in experimentally transfected mouse L cells. Low levels of hepatitis B e antigen (HBeAg) were detected from the L cells regardless of 5-azaC treatment, and synthesis of HBeAg was dependent on the growth state of the cultures. No HBcAg or HBeAg was detected in PLC/PRF/5 cells with or without 5-azaC treatment. This observation suggests that there is a distinct difference between experimentally transfected cells with HBV and the naturally derived material.
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PMID:Hepatitis B virus gene expression in two cell lines, one derived from a natural human infection, the other experimentally infected in vitro. 241 54


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