Project description:This SuperSeries is composed of the following subset Series: GSE41026: Expression analysis of HepG2, HepG2-slug and HepG2-slug on Matrigel GSE41027: Chip-chip from HepG2 cells and HepG2 cells with slug overexpression Refer to individual Series
Project description:Fructosamine-3-kinases (FN3Ks) are a family of metabolic kinases which are evolutionarily related to eukaryotic protein kinases. Aberrant regulation of these kinases by altered redox homeostasis is a major contributing factor in aging and disease. However, the mechanisms of regulation and cellular functions of these kinases are not known. Bioinformatic analyses of cancer cell lines identified significant overexpression of FN3K in liver and eye cancer cells. To assess the functional significance of this increased expression, a CRISPR knockout of FN3K (FN3K-KO) was generated in the HepG2 liver cancer cell line. The metabolome was compared between FN3K-KO and WT HepG2 cells using untargeted 1H NMR metabolomics. This revealed significant differences in several metabolites that suggest a role for FN3K in regulating redox and energy balance in HepG2 cells.
Project description:Our objective was to elucidate patterns of gene expression underlying the PBLD overexpression in HepG2 cells. The transcript profiles of PBLD overexpressed HepG2 cells were compared to the gene expression profiles of HepG2 cells control. Gene expression is compared at a global level using total RNA from PBLD overexpressed HepG2 cells and controls using the Illumina microarray platform.
Project description:To elucidate the principal downstream mediator responsible for USP18-mediated Sorafenib resistance in HCC, we conducted cluster analysis on the differential protein expression based on the whole-proteome analysis of HepG2 cells with or without overexpression of USP18 (HepG2-USP18-OE vs. HepG2-Ctrl), we identified 47 commonly downregulated proteins and 31 upregulated proteins .
Project description:In order to characterize the differentially expressed miRNAs after the p53 activation , small RNA-seq were used after the overexpression of p53 in HepG2 cells. Four samples of HepG2 cells were subjected to small RNA-seq in two biological replicates.The HepG2 cells were treated with 1µg/ml doxorubicin for 24 hours to induce the expression of p53. The experimental group(dox-treated HepG2ï¼HepG2_24h_rep1 and HepG2_24h_rep2) and control group(untreated HepG2: HepG2_0h_rep1 and HepG2_0h_rep2) were subjected to small RNA-seq to identify the p53-regulated miRNAs.
Project description:Our objective was to elucidate patterns of gene expression underlying the PBLD overexpression in HepG2 cells. The transcript profiles of PBLD overexpressed HepG2 cells were compared to the gene expression profiles of HepG2 cells control.