Project description:Genome wide expression changes following treatment with the HDACs (Histone Deacetylase Inhibitor) CG-1521 (7.5uM) or TSA (Trichostatin A) were investigated to determine regulatory targets and patterns of the HDAC Inhibitors. LNCaP Prostate Cancer cells were treated for a period of 24h with either CG-1521 (7.5uM) or TSA (5uM) following a 24h seeding period. At the selected time point, total RNA was harvested from the cells for hybridization and analysis by Nimblgen Systems Inc using the homo sapiens gene expression array.
Project description:Genome wide expression changes following treatment with the HDACs (Histone Deacetylase Inhibitor) CG-1521 (7.5uM) or TSA (Trichostatin A) were investigated to determine regulatory targets and patterns of the HDAC Inhibitors. Keywords: Expression response to treatment, data was used for a comparison of gene expression and regulation between CG-1521 and TSA in LNCaP Cells
Project description:This SuperSeries is composed of the following subset Series: GSE28542: Expression Profiling of Inflammatory Breast Cancer Cells Treated with the Novel Histone Deacetylase Inhibitor, CG-1521 (Affymetrix HuGene-1_0) GSE28543: Expression Profiling of Inflammatory Breast Cancer Cells Treated with the Novel Histone Deacetylase Inhibitor, CG-1521 (Agilent miRNA v12.0) Refer to individual Series
Project description:Human prostate cancer cells treated with shCSN5(sh37) or CSN5 inhibitior (CSN5i-3). Cells were treated with DMSO, 1uM (in C4-2), 5uM (in LNCaP, 22Rv1) or 10 uM (in PC3) CSN5i-3 for 48 hours. Cells were prepared for RNA-seq.
Project description:Studies of gene expression profiles using the whole genome wide microarray analysis in SUM149PT cells (ER-, p53mut) and SUM190PT cells (ER-, p53mut) when treated with 5 or 7.5 uM CG-1521 alone and in combination with 10 nM 17beta-estradiol. Comparisons between each treatment group provides evidence for the dysregulation of genes associated with the spindle assembly checkpoint. Three independent experiments were carried out in SUM149PT and SUM190PT cells, which were treated with vehicle (ethanol/DMSO), 10nM 17beta-estradiol, 5 or 7.5 uM CG-1521, and the combination of 17 beta-estradiol and CG-1521. Total RNA was extracted from cell lysates using QIAGEN RNeasy mini kit after 48h of treatment.
Project description:Studies of gene expression profiles using the whole genomewide microarray analysis of miRNA in SUM149PT cells (ER-, p53mut) and SUM190PT cells (ER-, p53mut) when treated with 5-7.5 µM CG-1521 alone and in combination with 10 nM 17β-Estradiol. Comparisons between each treatment group provides evidence for the dysregulation of miRNA affecting genes associated with the spindle assembly checkpoint. Four independent experiments were carried out in SUM149PT and SUM190PT cells, which were treated with vehicle (ethanol/DMSO), 10nM 17β-Estradiol, 5 or 7.5µM CG-1521, and the combination of 17β-Estradiol and CG-1521. Total RNA was extracted from cell lysates using QIAGEN miRNeasy mini kit after 48h of treatment.
Project description:We set out to identify early changes in gene expression in S. cerevisiae after treatment with the histone deacetylase inhibitor CG-1521. Exponentially growing yeast cells were treated with 50 μM CG-1521 or vehicle control for 1h. The experiment was performed in two independent biological replicates.
Project description:Histone deacetylase (HDAC) inibitors suppress cell proliferation of prostate cancer, but the detailed mechanisms are unknown. Moreover, HDAC includes 18 family members, namely HDAC1-11 and SIRT1-7, and differences of effects on prostate cancer proliferation among these enzymes are also unknown. Thus, we clarified differences of gene expression between prostate cancer cell line (LNCaP) treated with pan-HDAC inhibitors (TSA and OBP-801) or selective HDAC inhibitor (NCC-149, HDAC8-specific inhibitor)using cDNA microarray. LNCaP treated with TSA (1μM), NCC149 (2μM), OBP-801 (200nM) or DMSO for 24hrs, RNA was extracted from cells, and cDNA array was performed.
Project description:Transcriptional silencing associated with aberrant promoter hypermethylation is a common mechanism of inactivation of tumor suppressor genes in cancer cells. To profile the genes silenced by hypermethylation in prostate cancer, we screened an expression microarray for genes reactivated in the LNCaP, DU-145, PC-3 and MDA2b prostate tumor cell lines after treatment with the demethylating drug 5-aza-2 deoxycytidine (5Aza-dC) and histone deacetylation inhibiting drug trichostatin A (TSA).
