Human hepatoma Huh-7 cell culture models deficient in apolipoprotein B secretion
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ABSTRACT:
PROVIDER: PRJNA1124159 | ENA |
REPOSITORIES: ENA
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Project description:High plasma apolipoprotein B (apoB)-containing lipoproteins are both a biomarker and causal mediator of many metabolic diseases. Inhibition of apoB and MTP decreases plasma lipid levels but at a risk of lipid accumulation in tissues. Whole body knock out of MTP and APOB are embronically lethal. Therefore, we created a human hepatome cells line (Ako) deficient in APOB gene to understand the global consequences of APOB loss. APOB gene deletion significantly reduced apoB mRNA and protein levels in the Ako cells compared to control cells. These cells supported apoB48 secretion when transfected with apoB48 expression plasmids. These cells did not accumulate significant amounts of triglyceride. KEGG pathway analysis of RNA-Seq data showed a significant increase in DNA replication/repair pathway and complement/coagulation cascade in the Ako cells. The most downregulated pathways included the PI3k-Akt signaling and MAPK signaling pathways. Total proteome analysis of secretory proteins identifed Vitamin D binding protein as the most upregulated protein while apoB was the most dowregulated protein in these cells. Since both APOB and MTP are important part of the lipoprotein assmebly and secretion, we also perfrmed total transcriptome analysis for the MTP deficient Huh-7 (Mko-3) cells. We found differential expression of some the pathways in both Ako and Mko-3 cells such as DNA replication, base excision repair, steroid hormone biosynthesis and pathways reated to breast cancer. These cells may be useful in studying structure-function analysis of apoB peptides and to address the cellular consequences of disruptions in lipoprotein assembly and secretion. However; further detailed studies are needed to establish how apoB regulates these pathways
2025-07-23 | GSE269949 | GEO
Project description:Hepatitis C virus (HCV) is a global problem. To better understand HCV infection researchers employ in vitro HCV cell-culture (HCVcc) systems that use Huh-7 derived hepatoma cells that are particularly permissive to HCV infection. A variety of hyper-permissive cells have been subcloned for this purpose. In addition, subclones of Huh-7 which have evolved resistance to HCV are available. However, the mechanisms of susceptibility or resistance to infection among these cells have not been fully determined. In order to elucidate mechanisms by which hepatoma cells are susceptible or resistant to HCV infection we performed genome-wide expression analyses of six Huh-7 derived cell cultures (Huh-7, Huh-7.5.1, Huh-7.5.1c2, R1.09, R1.10 and R2.1) R that have different levels of permissiveness to infection. A great number of genes, representing a wide spectrum of functions are differentially expressed between cells. To focus our investigation, we identify host proteins from HCV replicase complexes, perform gene expression analysis of three HCV infected cells (infected Huh-7, Huh-7.5.1 and Huh-7.5.1c2) and conduct a detailed analysis of differentially expressed host factors by integrating a variety of data sources. Our results demonstrate that changes relating to susceptibility to HCV infection in hepatoma cells are linked to the innate immune response, secreted signal peptides and host factors that have a role in virus entry and replication. This work identifies both known and novel host factors that may influence HCV infection. Our findings build upon current knowledge of the complex interplay between HCV and the host cell, which could aid development of new antiviral strategies. Six Huh-7 derived hepatoma cell types that have different levels of susceptibility to HCV infection in cell culture are used: Huh-7, Huh-7.5.1, Huh-7.5.1c2, R1.09, R1.10 and R2.1. Of these the first three (label starting Huh are susceptible to HCV infection and the latter three (label starting R are resistant to HCV infection. All cell types are derived from Huh-7. Huh-7.5.1 is a subclone of Huh-7.5 that in turn is a subclone of Huh-7. Huh-7.5.1c2 is a subclone of Huh-7.5.1. R1.09 and R1.10 are subclones of R1 that is inturn a sublone of Huh-7.5,1. R2.1 is a subclone of Huh-7.5.1.
2011-06-11 | GSE29889 | GEO
Project description:Hepatitis C virus (HCV) is a global problem. To better understand HCV infection researchers employ in vitro HCV cell-culture (HCVcc) systems that use Huh-7 derived hepatoma cells that are particularly permissive to HCV infection. A variety of hyper-permissive cells have been subcloned for this purpose. In addition, subclones of Huh-7 which have evolved resistance to HCV are available. However, the mechanisms of susceptibility or resistance to infection among these cells have not been fully determined. In order to elucidate mechanisms by which hepatoma cells are susceptible or resistant to HCV infection we performed genome-wide expression analyses of six Huh-7 derived cell cultures (Huh-7, Huh-7.5.1, Huh-7.5.1c2, R1.09, R1.10 and R2.1) R that have different levels of permissiveness to infection. A great number of genes, representing a wide spectrum of functions are differentially expressed between cells. To focus our investigation, we identify host proteins from HCV replicase complexes, perform gene expression analysis of three HCV infected cells (infected Huh-7, Huh-7.5.1 and Huh-7.5.1c2) and conduct a detailed analysis of differentially expressed host factors by integrating a variety of data sources. Our results demonstrate that changes relating to susceptibility to HCV infection in hepatoma cells are linked to the innate immune response, secreted signal peptides and host factors that have a role in virus entry and replication. This work identifies both known and novel host factors that may influence HCV infection. Our findings build upon current knowledge of the complex interplay between HCV and the host cell, which could aid development of new antiviral strategies. Six Huh-7 derived hepatoma cell types that have different levels of susceptibility to HCV infection in cell culture are used: Huh-7, Huh-7.5.1, Huh-7.5.1c2, R1.09, R1.10 and R2.1. Of these the first three (label starting Huh are susceptible to HCV infection and the latter three (label starting R are resistant to HCV infection. All cell types are derived from Huh-7. Huh-7.5.1 is a subclone of Huh-7.5 that in turn is a subclone of Huh-7. Huh-7.5.1c2 is a subclone of Huh-7.5.1. R1.09 and R1.10 are subclones of R1 that is inturn a sublone of Huh-7.5,1. R2.1 is a subclone of Huh-7.5.1. 39 samples are used. In every case there are 3 biological replicates, i.e., there are 13 unique conditions (39/3=13). These samples are subdivided between two studies: (1) A comparison of HCV infection resistant cells R1.09, R1.10 and R2 against HCV susceptible Huh-7.5.1. (2) A comparison of JFH1 HCV infected Huh-7, Huh-7.5.1 and Huh-7.5.1c2 cells versus their uninfected counterparts. In each case there are two uninfected counterparts, cells that were harvested after being in culture for 20 hours and cells that were harvested at the same time point as the infected cells, that is, at the peak time of infection. Peak times for infection vary between cells, depending on their susceptibility to infection: 168 hours for Huh-7, 120 hours for Huh-7.5.1 and 96 hours for Huh-7.5.1c2.
2011-06-11 | E-GEOD-29889 | biostudies-arrayexpress
Project description:The expression profiling of HBV-transfected Huh-7 cells and control cells. Hepatocellular carcinoma (HCC) is one of major malignant disease worldwide, and patients with chronic hepatitis B virus (HBV) infection have a high risk of developing HCC. Via microarray gene expression analysis, we detected the gene alteration in HBV transfected hepatoma cells.
2016-06-18 | GSE83489 | GEO
Project description:Hepatitis B virus (HBV) infection could cause hepatitis, liver cirrhosis and hepatocellular carcinoma. HBV-mediated pathogenesis is only partially understood, but X protein (HBx) reportedly possesses oncogenic potential. Exosomes are small membrane vesicles with diverse functions released by various cells including hepatocytes, and HBV harnesses cellular exosome biogenesis and export machineries for virion morphogenesis and secretion. Therefore, HBV infection might cause changes in exosome contents with functional implications for both virus and host. In this project, exosome protein content changes induced by HBV and HBx were quantitatively analyzed by SILAC/LC-MS/MS. Exosomes prepared from SILAC-labeled hepatoma cell line Huh-7 transfected with HBx, wildtype or HBx-null HBV replicon plasmids were analyzed by LC-MS/MS.
2017-03-29 | MSV000080794 | MassIVE
Project description:Hepatitis B virus (HBV) infection could cause hepatitis, liver cirrhosis and hepatocellular carcinoma. HBV-mediated pathogenesis is only partially understood, but X protein (HBx) reportedly possesses oncogenic potential. Exosomes are small membrane vesicles with diverse functions released by various cells including hepatocytes, and HBV harnesses cellular exosome biogenesis and export machineries for virion morphogenesis and secretion. Therefore, HBV infection might cause changes in exosome contents with functional implications for both virus and host. In this project, exosome protein content changes induced by HBV and HBx were quantitatively analyzed by SILAC/LC-MS/MS. Exosomes prepared from SILAC-labeled hepatoma cell line Huh-7 transfected with HBx, wildtype or HBx-null HBV replicon plasmids were analyzed by LC-MS/MS.
2014-10-09 | PXD001339 | Pride
Project description:Apolipoprotein E2 protects against aging-induced neuronal endosomal dysfunction through enhanced exosome secretion
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Project description:Effect of knockdown of CENPU on gene expression of Huh-7 and MHCC-97H hepatoma cells
| PRJNA841635 | ENA
Project description:Sorafenib is the global standard of care for patients with advanced hepatocellular carcinoma. It has marginal efficacy and patients invariably develop therapeutic resistance. The primary goal of this project was to comprehensively chratcerize the molecular profile of sorafenib resistant Huh-7/SR1 and Huh-7/SR2 cells compared to their parental counterpart Huh-7 cells, and discover potential new druggable targets which can overcome sorafenib resistance.
2025-07-30 | GSE200098 | GEO
Project description:To investigate the function of CENPU in the regulation of hepatocellular carcinoma tumorigenesis , we established Huh-7 and MHCC-97H cell lines in which CENPU gene has been knocked down by siRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different cells.
2025-05-23 | GSE203625 | GEO