ABSTRACT: Expression Profiles of HepG2 cells treated with following compounds: Azathriopine, Furan, Tetradecanoyl phorbol acetate, Tetrachloroethylene, Diazinon and Dmannitol
Project description:The transcriptomic changes induced in the human liver cell line HepG2 by Azathriopine (250M-BM-5M, Sigma-Aldrich), Furan (2mM, Sigma-Aldrich), Tetradecanoyl phorbol acetate (500nM, Sigma-Aldrich), Tetrachloroethylene (2mM, Sigma-Aldrich), Diazinon (250M-BM-5M, Sigma-Aldrich) and Dmannitol (250M-BM-5M, Sigma-Aldrich) during 4, 8, 24, 48 and 72hrs As a solvent control for Azathriopine, Furan, Diazinon and Tetradecanoyl phorbol acetate, DMSO was used (0.5%); As a solvent control for tetrachloroethylene, ethanol was used (0.5%); As a solvent control for D-mannitol, HBSS was used (0.5%) The study investigated differential gene expression in HepG2 cell line mRNA following 4, 8, 24, 48 and 72h hours of exposure to Azathriopine, Furan, Tetradecanoyl phorbol acetate, Tetrachloroethylene, Diazinon, D-mannitol, DMSO solvent control, ethanol solvent control and HBSS solvent control. Three biological replicates per compound/solvent. In total 135 arrays were analyzed in total.
Project description:The transcriptomic changes induced in the human liver cell line HepG2 by Azathriopine (250µM, Sigma-Aldrich), Furan (2mM, Sigma-Aldrich), Tetradecanoyl phorbol acetate (500nM, Sigma-Aldrich), Tetrachloroethylene (2mM, Sigma-Aldrich), Diazinon (250µM, Sigma-Aldrich) and Dmannitol (250µM, Sigma-Aldrich) during 4, 8, 24, 48 and 72hrs As a solvent control for Azathriopine, Furan, Diazinon and Tetradecanoyl phorbol acetate, DMSO was used (0.5%); As a solvent control for tetrachloroethylene, ethanol was used (0.5%); As a solvent control for D-mannitol, HBSS was used (0.5%)
Project description:From the result of comparative the gene expression analyses of human hepatoma cell line, HepG2 following exposures of three heavy metals; arsenic, cadmium and nickel and three carcinogens; N-dimethylnitrosoamine (DMN), 12-O-tetradecanoylphorbol-13-acetate (TPA) and tetrachloroethylene (TCE), 31-55% of the genes altered by As, Cd and Ni exposure were overlapped with those by three model carcinogen exposures in our experiments. In particular, three heavy metals shared certain characteristics with TPA and TCE in remarkable up-regulations of the genes associated with progression of cell cycle, which might play a central role in heavy metal carcinogenesis. In addition, this characteristic of gene expressions alteration was counteracted by intracellular accumulation of vitamine C in As-exposed cells but not in Cd- and Ni-exposed cells. These results suggest that the cell proliferative responses are caused by reactive oxygen species mainly in As exposure, while other mechanisms would be involved in these responses in Cd and Ni exposures. Experiment Overall Design: In this study, we examined the gene expression alteration in human hepatoma cell line, HepG2 following exposures of three heavy metals; arsenic, cadmium and nickel and three carcinogens; N-dimethylnitrosoamine (DMN), 12-O-tetradecanoylphorbol-13-acetate (TPA) and tetrachloroethylene (TCE) using DNA microarray with 8795 human genes. Furthermore, we also performed the DNA microarray analyses for the heavy metal exposed-cells that were loaded with vitamine C beforehand to examine the effects of antioxidant molecule to heavy metal exposures.
Project description:Gene expression profiling was analyzed using A549 cells that were treated with glucose deprivation (GD) or GD + phorbol-12-myristate-13-acetate (PMA).
Project description:Transcriptome analysis of the human monocytic cell line THP1 (ATCC TIB-202) treated or not with phorbol myristate acetate (PMA) +/- lipopolysaccharides-lipopolysaccharides binding protein (LPS-LBP)
Project description:So far, we have found phorbol 12-myristate 13-acetate (PMA) induced ubiquitin specific peptidase (USP) 2b isoform in myeloid leukemia cell lines such as HL60, THP-1, and U937. HL60, THP-1, and U937 undergoes differentiation into macrophage-like cells after stimulation with phorbol ester. To explore molecular function of USP2 in macrophages especially during lipopolysaccharide(LPS) response, we assess expression profiles of HL60-derivatives continuously expressing shRNA for USP2 and control shRNA.
Project description:So far, we have found phorbol 12-myristate 13-acetate (PMA) induced ubiquitin specific peptidase (USP) 2b isoform in myeloid leukemia cell lines such as HL60, THP-1, and U937. HL60, THP-1, and U937 undergoes differentiation into macrophage-like cells after stimulation with phorbol ester. To explore molecular function of USP2 in macrophages especially during lipopolysaccharide(LPS) response, we assess expression profiles of HL60-derivatives continuously expressing shRNA for USP2 and control shRNA.
Project description:We developed a general approach to small molecule library screening called GE-HTS (Gene Expression-Based High Throughput Screening) in which a gene expression signature is used as a surrogate for cellular states and applied it to the identification of compounds inducing the differentiation of acute myeloid leukemia cells. In screening 1,739 compounds, we identified 8 that reliably induced the differentiation signature, and furthermore yielded functional evidence of bona fide differentiation. This data set contains HL-60 cells treated in a time course, in replicate, with 1 uM all trans retinoic acid (ATRA) and 10 nM phorbol 12-myristate 13-acetate (PMA). Also included are untreated HL-60 controls. This data set was used to select marker genes that distinguish the undifferentiated from the PMA or ATRA differentiated states. Keywords = AML Keywords = leukemia Keywords = HL-60 Keywords = chemical genomics Keywords: repeat sample
