BioProject

Treatment of the acute T cell leukemia cell line Jurkat in vitro with the most potent histone deacetylase inhibitor, Trichostatin A induced apoptosis in a dose-dependent manner. More...

Treatment of the acute T cell leukemia cell line Jurkat in vitro with the most potent histone deacetylase inhibitor, Trichostatin A induced apoptosis in a dose-dependent manner. Analysis of the drug-treated Jurkat cells using high throughput genome-wide gene expression profiling indicated the upregulation as well as downregulation of several genes crucial for cellular functions. Use of quantitative reverse transcriptase-mediated polymerase chain reaction validated the regulation of selected genes in drug-treated cells. Collectively, this study has unraveled the genes involved in epigenetic regulation of the T cell leukemia. Microarray analysis was performed to determine the changes in global gene expression profiles during apoptosis of a T cell leukemia induced by the histone deacetylase inhibitor, Trichostatin A. Drug treatment induced the upregulation and repression of a number of genes. Overall design: The T cell leukemia cell line Jurkat was grown in tissue culture, resuspended at 1 x 106 cells/ml and treated with Trichostatin A dissolved in dimethylsulfoxide at 50 ng/ml concentration. Controls included untreated cells and those treated with an equal amount of the vehicle. After 18 hours of culture, cells were harvested, and total RNA was extracted and hybridized to microchips in duplicate. Differential gene expression was analyzed as follows: media control vs. DMSO-treated cells, and media control vs. Trichostatin A-treated cells. Less...