scholarly journals Inhibitory effect of parvovirus H-1 on the formation of colonies of human hepatoma cell line in vitro and its tumors in nude mice

Cell Research ◽  
1994 ◽  
Vol 4 (1) ◽  
pp. 47-56 ◽  
Author(s):  
Shangjun Yan ◽  
Chengwu Ma ◽  
Xianhua Chen ◽  
Shanhong Wan ◽  
Zuyu Luo
Keyword(s):  
Cell Line ◽  
Nude Mice ◽  
Hepatoma Cell ◽  
Inhibitory Effect ◽  
Hepatoma Cell Line ◽  
Human Hepatoma ◽  
Human Hepatoma Cell ◽  
Human Hepatoma Cell Line

scholarly journals Cell Clones Selected from the Huh7 Human Hepatoma Cell Line Support Efficient Replication of a Subgenomic GB Virus B Replicon

2002 ◽  
Vol 76 (15) ◽  
pp. 7736-7746 ◽  
Author(s):  
Amedeo De Tomassi ◽  
Maura Pizzuti ◽  
Rita Graziani ◽  
Andrea Sbardellati ◽  
Sergio Altamura ◽  
...  
Keyword(s):  
Host Cell ◽  
Cell Line ◽  
Hepatoma Cell ◽  
Hepatoma Cell Line ◽  
Human Hepatoma ◽  
Human Hepatoma Cell ◽  
Subgenomic Rna ◽  
Human Hepatoma Cell Line ◽  
Huh7 Cells

ABSTRACT Tamarins (Saguinus species) infected by GB virus B (GBV-B) have recently been proposed as an acceptable surrogate model for hepatitis C virus (HCV) infection. The availability of infectious genomic molecular clones of both viruses will permit chimeric constructs to be tested for viability in animals. Studies in cells with parental and chimeric constructs would also be very useful for both basic research and drug discovery. For this purpose, a convenient host cell type supporting replication of in vitro-transcribed GBV-B RNA should be identified. We constructed a GBV-B subgenomic selectable replicon based on the sequence of a genomic molecular clone proved to sustain infection in tamarins. The corresponding in vitro-transcribed RNA was used to transfect the Huh7 human hepatoma cell line, and intracellular replication of transfected RNA was shown to occur, even though in a small percentage of transfected cells, giving rise to antibiotic-resistant clones. Sequence analysis of GBV-B RNA from some of those clones showed no adaptive mutations with respect to the input sequence, whereas the host cells sustained higher GBV-B RNA replication than the original Huh7 cells. The enhancement of replication depending on host cell was shown to be a feature common to the majority of clones selected. The replication of GBV-B subgenomic RNA was susceptible to inhibition by known inhibitors of HCV to a level similar to that of HCV subgenomic RNA.

scholarly journals Effects of Fresh Royal Jelly on the Proliferation of Human Hepatoma Cell Line SMMC-7721

1970 ◽  
Vol 1 (2) ◽  
Author(s):  
Mingmin Wang
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Line ◽  
Royal Jelly ◽  
Hepatoma Cell ◽  
Inhibitory Effect ◽  
Hepatoma Cell Line ◽  
Dependent Manner ◽  
Human Hepatoma ◽  
Human Hepatoma Cell ◽  
Human Hepatoma Cell Line

Objective: To investigate the effect of fresh royal jelly on the proliferation of human hepatoma cell line SMMC-7721. Methods: We found that the administration of fresh royal jelly could alleviate the condition of hepatocellular carcinoma patients in a certain extent. The human hepatocellular carcinoma cell line SMMC-7721 was cultured in vitro. MTT colorimetric method was used to treat fresh cells and serum containing human serum. The effect of SMMC-7721 proliferation was observed. Results: The aqueous solution of fresh royal jelly had a certain effect on the proliferation of hepatoma cell line SMMC-7721 in a dose-dependent manner. The serum containing fresh royal jelly could inhibit the proliferation of human hepatoma cell line SMMC-7721, and its inhibitory effect showed dose-dependent. Conclusion: The serum containing fresh royal jelly has a significant inhibitory effect on the proliferation of human hepatoma cell line SMMC-7721 and its anti-cancer effect may be derived from its metabolites or stimulating the formation of immune-reactive substances in the body, in which in the clinical treatment of liver cancer and research have a certain value.

scholarly journals In Vivo and In Vitro Effect of a Nutrient Mixture on Human Hepatoma Cell Line SK‐Hep‐1

2007 ◽  
Vol 21 (6) ◽  
Author(s):  
M. Waheed Roomi ◽  
Vadim Ivanov ◽  
Aleksandra Niedzwiecki ◽  
Matthias Rath
Keyword(s):  
Cell Line ◽  
Hepatoma Cell ◽  
Hepatoma Cell Line ◽  
Human Hepatoma ◽  
Human Hepatoma Cell ◽  
Human Hepatoma Cell Line ◽  
Vitro Effect

scholarly journals Synthetic peptides from the circumsporozoite proteins of Plasmodium falciparum and Plasmodium knowlesi recognize the human hepatoma cell line HepG2-A16 in vitro.

1986 ◽  
Vol 164 (6) ◽  
pp. 1915-1922 ◽  
Author(s):  
S B Aley ◽  
M D Bates ◽  
J P Tam ◽  
M R Hollingdale
Keyword(s):  
Cell Line ◽  
Plasmodium Knowlesi ◽  
Hepatoma Cell ◽  
Hepatoma Cell Line ◽  
Human Hepatoma ◽  
Repeat Region ◽  
Human Hepatoma Cell ◽  
Human Hepatoma Cell Line ◽  
Hepatoma Cell Line Hepg2

Several lines of evidence have emphasized the importance of the malaria circumsporozoite (CS) protein as a factor in sporozoite invasion of the hepatocyte; however, the specific mechanism of cell recognition and invasion has not been explained. In this study we present evidence that a highly conserved region of the CS protein immediately adjacent to the repeat region, the N1 region, specifically recognizes receptors on the human hepatoma cell line HepG2-A16 under conditions where invasion by sporozoites can occur. Peptides consisting of sequences from the repeat region or of the more extensive N2 region showed no such specific association. Antibody against the N1 peptide could inhibit sporozoite invasion in vitro. Covalent coupling of radiolabeled N1 peptide to HepG2-A16 cells identified two hepatic cell proteins to be closely associated with the peptide. We suggest that these proteins could act as receptors or mediators, via the N1 region of the CS protein, for the P. falciparum sporozoite in the process of invasion of the hepatocyte.

Abstract 418: Bifunctional Role of Autophagy in Intracellular ApoB Degradation and Lipid Droplet Mobilization

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Patricia Christian ◽  
Mostafa Zamani ◽  
Wei Qui ◽  
Rianna Zhang ◽  
Khosrow Adeli
Keyword(s):  
Cell Line ◽  
Hepg2 Cells ◽  
Ex Vivo ◽  
Hepatoma Cell ◽  
Hepatoma Cell Line ◽  
Human Hepatoma ◽  
Human Hepatoma Cell ◽  
Human Hepatoma Cell Line ◽  
Vldl Assembly

Introduction: As apolipoprotein B (apoB) is translated and translocated into the ER, lipids from cytoplasmic lipid droplets (LDs) are added to promote folding and to initiate very-low-density-lipoprotein (VLDL) assembly. However, without sufficient lipid availability, apoB is misfolded and subject to proteasomal degradation. Evidence now shows that apoB can also be degraded through autophagy under certain conditions, and that LDs are also subject to autophagic degradation, a process referred to as lipophagy. We postulate that apoB autophagy and LD lipophagy integrate to regulate hepatic lipid export and VLDL production. Methods/Results: Studies were conducted in vitro using the human hepatoma cell line, HepG2 and ex vivo using primary Syrian Golden hamster hepatocytes. Cells were fat loaded with/without 0.4 mM OA for 4 hours and simultaneously treated with an autophagy inhibitor 3-methyadenine (3-MA; 100uM) or an autophagy inducer, Torin 1 (250nM). HepG2 cells were transfected with 10 nM of atg12 siRNA, an essential autophagy related gene, for a total of 72 hours. In freshly isolated primary hamster hepatocytes, inhibition of autophagosome formation, through treatment with 3-MA, significantly increased cellular levels of newly synthesized apoB, without a significant increase in apoB secreted into the media. Interestingly, treating these cells with Torin 1 to promote autophagy also significantly increased apoB recovery. However, modulation of autophagy activity also affected the average number of LDs per cell, indicating that lipophagy activity had also been modified, potentially affecting VLDL formation. Conversely, while inhibition and induction of autophagy in HepG2 cells, a human hepatoma cell line, reduced and increased apoB co-localization with autophagosomes respectively, siRNA knockdown of atg12 as well as 3-MA treatment decreased apoB recovery. However, this did not appear to be due to reduction in LD breakdown through autophagy. The data obtained with primary hamster hepatocytes suggest that autophagy may play a dual role in VLDL assembly in vivo by regulating both degradation of apoB and lipidation of VLDL particles through mobilization of lipid from LDs. Defects in these pathways can induce hepatic LD accumulation and steatosis.

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