Project description:Many reports shows that DEPDC1 is up-regulated in many tumor types and promotes cell proliferation and invasion, thereby functioning as an oncogene. Hepatocellular Carcinoma has been shown to overexpress DEPDC1, and up-regulated DEPDC1 associates with poorer prognosis.In addition, we found that DEPDC1 knockdown significantly inhibited HCC cell proliferation, colony formation and migration. In order to investigate the mechanism of DEPDC1 in regulating HCC progression, we performed gene array analysis.
Project description:To investigate the role for LSD1 under hypoxia condition. we depleted LSD1 gene with siRNA in Huh-1 cell lines under 1% O2 hypoxia condtion, and than perforemed gene expression microarray analysis. Using Gene Set Enrichment Analysis (GSEA), determined to identify the biological pathway.
Project description:To investigate the role for LSD1 under hypoxia condition. we depleted LSD1 gene with siRNA in Huh-1 cell lines under 1% O2 hypoxia condtion, and than perforemed gene expression microarray analysis. Using Gene Set Enrichment Analysis (GSEA), determined to identify the biological pathway. Determined the gene expression profile of the LSD konckdown effect under hypoxia condition. Using Gene Set Enrichment Analysis (GSEA) decided to identify the biological pathways.
Project description:Transcriptional profiling of human hepatocarcinoma comparing Huh-7 and SNU-739. Two-condition experiment, normalized ratio represented by Huh-7/SNU-739. Biological replicates: 2 Huh-7 replicates, 2 SNU-739 replicates.
Project description:Nucleus pulposus cells (NPCs) were used to examine the effect of LINC02569, a novel lncRNA. In particular, its effect in intervertebral disc degeneration was determined. Treatment of LINC02569 siRNA (si-02569) was to be compared with negative control siRNA (si-NC).
Project description:To clarify the molecular mechanism by which FNDC4 promotes HCC invasion, mass spectrometry (MS) analysis was performed on the lysates of Huh-7-overexpressing FNDC4 and normal Huh-7 cells.
Project description:We transfected siRNA-EIF4G2 and si-NC into Hep3B cells to explore the differentially expressed genes in cells and the affected intracellular signaling pathways after EIF4G2 knockdown
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.
Project description:Small nucleolar RNAs (snoRNAs) dysfunction have been associated with cancer development. We investigated the function of an orphan C/D box class snoRNA, SNORD126, in hepatocellular carcinoma (HCC) and colorectal cancer (CRC) cells We used microarrays to identify targets with roles in SNORD126âs activity in Huh-7 cells SNORD126- or EGFP-overexpressed Huh-7 cells were collected and followed by RNA extraction, then hybridized with Affymetrix microarrays. We sought to obtain the differentially expressed genes between the two groups.
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.