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 the flavonoids from Scutellaria baicalensis Georgi (baicalein, baicalin and wogonin) in cultured human hepatoma cells (Hep G2, Hep 3B and SK-Hep1) were compared by MTT assay and flow cytometry. All three flavonoids dose-dependently decreased the cell viabilities accompanying the collapse of mitochondrial membrane potential and the depletion of glutathione content. However, the influence of baicalein, baicalin or wogonin on cell cycle progression was different. All three flavonoids resulted in prominent increase of G2/M population in Hep G2 cells, whereas an accumulation of sub G1 (hypoploid) peak in Hep 3B cells was observed. In SK-Hep1 cells, baicalein and baicalin resulted in dramatic boost in hypoploid peak, but wogonin made mainly in G1 phase accumulation. These data, together with the previous findings in other hepatoma cell lines, suggest that baicalein, baicalin and wogonin might be effective candidates for inducing apoptosis or inhibiting proliferation in various human hepatoma cell lines.
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PMID:Different effects of baicalein, baicalin and wogonin on mitochondrial function, glutathione content and cell cycle progression in human hepatoma cell lines. 1185 62

Steaming ginseng at high temperature increased its cytotoxicity to SK-Hep-1 hepatoma cancer cells. HPLC separation and fractionation followed by MTT assay revealed that ginsenosides Rg3, Rg5, Rk1, Rs5, and Rs4 are the active principles. Their 50% growth inhibition concentration (GI50) values were 41, 11, 13, 37, and 13 microM, respectively. Cisplatin had a GI50 of 84 microM in the same assay conditions.
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PMID:Cytotoxic dammarane glycosides from processed ginseng. 1196 5

The effect of howiinol A (GHM-10) on the growth of several cancer and normal cells were studied, using the methods of cell growth curve determination, MTT test and soft-agar colony formation assay. The results showed that GHM-10 exhibited potent inhibitory effect on cancer cells with an IC50 of 2 micrograms.ml-1 approximately. Normal cells, especially bone marrow progenitor cells, were shown to be less sensitive to GHM-10. A drug-resistant cell line, KB/VCR200, was found to be as sensitive as its parental KB cells. GHM-10 did not induce HL-60 cell differentiation. In murine transplantable tumors, GHM-10 was found to have significant therapeutic effect on mice bearing solid tumor hepatoma H22, Lewis lung carcinoma and S180 ascites.
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PMID:[Studies on the anticancer effect of howiinol A, a new compound isolated from Goniothalamus howii]. 1201 81

Primary hepatocellular carcinoma(HCC) is one of the common malignant tumors in China. In our previous work, a gene named fup1(function-unknown protein 1) was isolated that was expressed differently in HCC and in normal liver. We assumed that it might be a candidate oncogene for the HCC. The fup1 gene had a ORF of 1 233 bp, encoding a protein with M(r) of 46 kD and isoelectric point of 5.48. The sequence characteristics showed its possible localization in nuclei. Northern blots showed that this gene was weakly expressed in many types of human tissues, except in the heart, implying its tissue-specific expression pattern. MTT assay of the NIH 3T3 cells transfected with this gene in the form of recombinant eukaryotic expression plasmid showed its enhancing role to cellular proliferation.
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PMID:Cloning and Characterization of fup1, A Gene Highly Expressed in Hepatocellular Carcinoma. 1205 Aug 6

Melatonin, the major secretory product of the pineal gland, is in focus of many research areas because of its ability to scavenge free oxygen radicals and thereby protect cells and tissues from radical damage. Some studies suggest melatonin may be a possible therapeutic agent with potential clinical applications against pathological states due to reactive oxygen species. Here, we investigated the effects of melatonin on the mouse hepatoma cell line HEPA 1-6, coincubated with ethanol, and tamoxifen, respectively. Cell proliferation rates were detected by the 3-[4,5 dimethylthiazol-2-y1]-2,5-diphenyltetrazolium bromide (MTT) proliferation assay. A dose-dependent inhibition of the proliferative activity by melatonin was observed from 640 microM to 3 mM, which was significantly higher (P < 0.01) than with the solvent (ethanol) alone. Concentrations of 320 microM and less had no effect on cell proliferation. This antiproliferative effect might be because of the prolonged activation of mitogen-activated protein kinase which was activated by phosphorylation 15 min after the induction with melatonin. Furthermore, apoptosis was found to be enhanced by melatonin (75% more than with the solvent alone, P < 0.001). Finally, we show that the inhibitory effect of tamoxifen (25 microM) is markedly enhanced by the coincubation with melatonin (1.3 mM) up to 75% (P < 0.001). These data show that the antiproliferative effects of tamoxifen and ethanol, respectively, on mouse hepatoma cell line HEPA 1-6 are enhanced by melatonin. Although at the conditions described here the antiproliferative effects of melatonin occur at supraphysiological concentrations, these data may help to support clinical studies where melatonin is given simultaneously with tamoxifen or other standard chemotherapeutica.
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PMID:Potentiation of antiproliferative effects of tamoxifen and ethanol on mouse hepatoma cells by melatonin: possible involvement of mitogen-activated protein kinase and induction of apoptosis. 1212 80

Shuttle plasmid containing HSV-tk gene and regulatory sequence of the afp gene was constructed and recombined with the right arm of adenovirus DNA. The recombinant adenovirus vector was named pAdrAFPTK. Meanwhile, an AdCMVTK was constructed as control in which the tk gene was controlled under CMV promoter. PCR and Southern blot analyses were used to identify positive plaques. Virus titer was about 1x10(15) pfu/L determined by plaque forming assay. The AFP-positive cells or AFP-negative cells were infected with AdCMVTK or AdrAFPTK and then treated with GCV, respectively. Cytotoxic effects were assayed with MTT method. The IC(50) of GCV for both HeLa cells or BRL-3A cells (both were AFP-negative cells) and HepG2 cells (AFP-positive cells) were 1.3 &mgr;mol/L, 2&mgr;mol/L and <1&mgr;mol/L, respectively, after infection with AdCMVTK (m.o.i.=100). However, in the cases of infection with AdrAFPTK (m.o.i.=100), IC(50) were 1 000 &mgr;mol/L, >1 000 &mgr;mol/L and <1&mgr;mol/L for HeLa cells, BRL-3A cells and HepG2 cells, respectively. Results showed that this vector possessed advantages of high title, high infectivity coming from adenovirus and the character of cell type-specificity gene expression. The AdrAFPTK/GCV system may become a new, potent and specific approach for the gene therapy of the primary hepatoma.
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PMID:Specific Expression of Suicide Gene in Liver Cancer Cells Mediated by Adenovirus. 1216 32

An increased level of glucocorticoid receptors has been found in hepatoma. The aim of this study was to determine the in vivo effect of glucocorticoid on the growth of murine hepatoma cells. In vitro cell growth was determined by MTT assay, while cell cycle progression was assayed with flow cytometry. For in vivo experiments, ML-3 and Hepa 1-6 cells were implanted in BALB/c and SCID mice, respectively. Each mouse received 4 subcutaneous injections of hydrocortisone and/or RU486 after tumor implantation. We found that glucocorticoid treatment of ML-3 and Hepa 1-6 cells in vitro resulted in an increase in cell growth which was partially inhibited by RU486, a glucocorticoid antagonist. Glucocorticoid treatment enhanced the cell cycle progression of ML-3 cells. The incidence of ML-3 tumor in the hydrocortisone group was significantly higher than that of the saline, RU486, or hydrocortisone plus RU486 groups. RU486 partially blocked the hydrocortisone-stimulated growth of hepatoma. Further study showed that glucocorticoid treatment of SCID mice also stimulated Hepa 1-6 tumor growth. In conclusion, our results indicated that glucocorticoid directly stimulated hepatoma growth and this stimulation was not the result of immune suppression. Glucocorticoids may play an important role in regulating the growth of hepatoma.
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PMID:In vivo and in vitro growth stimulation of murine hepatoma cells by glucocorticoid. 1216 18

Recent studies have shown increased levels of cyclooxygenase-2 (COX-2) in a variety of human malignancies, including hepatocellular carcinoma (HCC), but so far it is unknown whether COX-2 contributes to the malignant growth and whether inhibition of COX-2 function modifies the malignant potential of liver tumors. COX-1 and COX-2 expression was determined in 4 liver tumor cell lines (Hep 3B, HuH-7, Hep G2, Sk-hep1) by Northern hybridization and Western immunoblot. The functional effects of the nonselective inhibitor sulindac sulfide and the COX-2 selective inhibitors SC-58635 and meloxicam were examined by 3(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazoliumbromide (MTT)-assays and BrdU uptake, morphology, and TUNEL analysis of apoptosis. Apoptosis regulating proteins were analyzed by Western immunoblot. COX-1 and COX-2 expression was demonstrable in all tested liver tumor cell lines. Sulindac sulfide (50 to 400 micromol/L), SC-58635 (6,25 to 400 micromol/L), and meloxicam (6.25 to 400 micromol/L) led to a significant time- and dose-dependent reduction of cell numbers of up to 80% (P <.05). At equimolar concentrations the effect was more pronounced when COX-2 was selectively blocked. COX-2 inhibition induced apoptosis and reduced tumor cell proliferation. Apoptosis after COX-2 inhibition with SC-58635 (50 micromol/L) was independent of BCL-2, BAX, and the phosphorylation status of AKT/PKB and BAD, but correlated with activation of caspase-9, caspase-3, and caspase-6. In conclusion, selective inhibition of COX-2 leads to a marked growth inhibition of human liver tumor cells, based on the induction of apoptosis and inhibition of proliferation and, thus, may offer therapeutic and preventive potential in human hepatocarcinogenesis.
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PMID:Proapoptotic and antiproliferative potential of selective cyclooxygenase-2 inhibitors in human liver tumor cells. 1229 35

Treatment of hepatocellular carcinomas (HCCs) with chemotherapy has generally been disappointing and it is most desirable to have more effective new drugs. We extracted and purified 6 xanthone compounds from the rinds (peel) of the fruits of Garcinia mangostana L., using partitioned chromatography and then tested the cytotoxic effects of these compounds on a panel of 14 different human cancer cell lines including 6 hepatoma cell lines, based on the MTT method. Several commonly used chemotherapeutic agents were included in the assay to determine the relative potency of the potential new drugs. Our results have shown that one of the xanthone derivatives which could be identified as garcinone E has potent cytotoxic effect on all HCC cell lines as well as on the other gastric and lung cancer cell lines included in the screen. We suggest that garcinone E may be potentially useful for the treatment of certain types of cancer.
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PMID:Garcinone E, a xanthone derivative, has potent cytotoxic effect against hepatocellular carcinoma cell lines. 1245 86

The stimulatory activity of human alpha-fetoprotein (AFP) on the growth of mouse hepatoma-22 cells had been reported in our previous paper. The present work aimed at further investigation of the effect of AFP on human hepatoma cell growth by MTT colorimetric assay. The results showed that AFP could stimulate the growth of SMMC-7721 human hepatoma cells in vitro. The present results also showed that the stimulatory effect of AFP on the growth of SMMC-7721 cells was decreased by the anti-serum of AFP. The anti-AFP antibody alone could suppress the growth of SMMC-7721 cells. On the other hand, AFP and anti-AFP antibody had no effect on the growth of HL-60 human leukemia cells, indicating that the tumor cell growth stimulating effect of AFP was not simply due to non-specific addition of exogenous protein and this effect of AFP showed strict tumor cell specificity. In addition, MCF-7 human breast cancer cell growth was also promoted by AFP and inhibited by anti-AFP antibody. Because AFP cell-surface receptors have been detected in MCF-7 breast cancer cells, and AFP could also be produced and secreted by MCF-7 cells, the possibility may be considered: AFP may bind with its receptors on tumor cell membrane for the purposes of growth stimulation.
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PMID:[Effect of alpha-fetoprotein on the growth of human hepatoma cells in vitro]. 1254 90


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