Project description:LNCaP cells are an established androgen receptor expressing prostate carcinoma cell line. Human foreskin fibroblasts also expressing the androgen receptor were obtained from phenotypic normal male individuals. Cells were cultured either at confluency leading to G0 cell cycle state or while they were proliferating. Cells were either untreated, or treated with dihydrotestosterone (DHT) or ethanol (ETOH) which also served as the solvent for the DHT. All experimental RNA samples derived from the untreated or treated cell lines were hybridized on cDNA arrays against a common reference. This reference was composed out of common reference CRG (50%) and out of fibroblast RNA (50%). This reference is also called "mixed reference" in the description of the 26 individual experiments. A strain or line experiment design type assays differences between multiple strains, cultivars, serovars, isolates, lines from organisms of a single species. Compound Based Treatment: dihydrotestosterone (DHT) or ethanol (ETOH = solvent) Cell Line: genital fibroblast cell line or prostate carcinoma cell line (LNCaP) Culture Synchrony: Go or proliferation Keywords: strain_or_line_design
Project description:The text description is: LNCaP are androgen receptor expressing prostate carcinoma cells. Genital skin fibroblasts also express the androgen receptor. Cells were either proliferating or they were G0-arrested. Treatment of cells was performed with either the androgen DHT (dihydrotestosterone), the androgen analogue R1881 (methyltrienolone), or the solvent ethanol. Some hybridizations were performed in the type 1 design. In these cases, the hormone treated sample was hybridized against the ethanol treated sample on the same microarray. Hormone mediated induction or repression of gene transcription can directly be deduced from R/G normalized ratios on arrays. For other experiments, the ethanol treated control and the hormone treated experiment were hybridized on separate microarrays against a common reference of RNA. This reference was composed out of common reference batch CRG (50%) and a fibroblast RNA (50%). This reference was called mixed reference. For all experiments, the same batch of mixed reference was used. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Compound Based Treatment: Ethanol, R1881 (methyltrienolone), or DHT (dihydrotestosterone) Cell Line: LNCaP (prostate cancer) or foreskin fibroblasts Culture Synchrony: proliferation / Go-arrest Keywords: compound_treatment_design
Project description:This study aimed to identify the mode of action of Schisandra chinensis water extracts (SCW) and Schisandra chinensis ethanol extracts (SCE) in SW1783 cell line.
Project description:LNCaP cells are an established androgen receptor expressing prostate carcinoma cell line. Human foreskin fibroblasts also expressing the androgen receptor were obtained from phenotypic normal male individuals. Cells were cultured either at confluency leading to G0 cell cycle state or while they were proliferating. Cells were either untreated, or treated with dihydrotestosterone (DHT) or ethanol (ETOH) which also served as the solvent for the DHT. All experimental RNA samples derived from the untreated or treated cell lines were hybridized on cDNA arrays against a common reference. This reference was composed out of common reference CRG (50%) and out of fibroblast RNA (50%). This reference is also called "mixed reference" in the description of the 26 individual experiments. A strain or line experiment design type assays differences between multiple strains, cultivars, serovars, isolates, lines from organisms of a single species. Compound Based Treatment: dihydrotestosterone (DHT) or ethanol (ETOH = solvent) Cell Line: genital fibroblast cell line or prostate carcinoma cell line (LNCaP) Culture Synchrony: Go or proliferation Computed
Project description:Desulfovibrio vulgaris has been studied extensively for its potential in the bioremediation of heavy metals and radionuclides. Hydrocarbons and solvents, as frequent environmental co-contaminants, have been reported to inhibit microbial activities and thereby pose a limitation on bioremediation efficiency. As a part of the Genomes: GTL project to deduce the stress response pathways in metal/radionuclide reducing bacteria, we studied the responses of D. vulgaris to ethanol, which is a solvent and co-contaminant frequently encountered at contaminated DOE sites. Growth experiments in closed vessels at 37 °C indicated that D. vulgaris could maintain normal growth with 1%(v/v) ethanol. The growth rates were reduced with increasing ethanol concentrations at 2% and 5%. Growth ceased when ethanol concentration was raised to 5%(v/v). Cell lysis was apparent with decreasing optical density following 10% ethanol addition. To assess the mechanism of ethanol inhibition, genome-wide transcriptional profiles were analyzed from D. vulgaris cultures following ethanol (5% v/v) treatment using whole-genome microarrays. The ethanol treatment altered the expression of a large number of genes in the D. vulgaris genome, of which 354 were up-regulated greater than 2 fold and 217 were down-regulated by over 2 fold. As expected, changes in the transcriptional profile were similar to those of the stress response to acetone, which is also a solvent. Transcripts highly up-regulated included genes encoding the flagella structural subunits, suggesting motility as a mechanism of solvent stress response. Another group of genes highly induced were chaperones, such as dnaJ, groES, and hsp20, indicating the importance of maintaining proper protein folding under ethanol stress. Down-regulated genes included two groups of genes, ribosomal proteins and amino acid transporters, consistent with the growth inhibition by ethanol observed in growth studies. These results were interpreted that D. vulgaris responds to elevated solvent levels by increased motility and maintenance of proper protein functions. Current work is focused on the analysis of regulatory pathways based on temporal transcriptional dynamics. Keywords: Stress response