Project description:Estrogen-responsive genes were identified by transcript profiling of estrogen-treated MCF-7 breast cancer cells. The gene expression profile generated after estrogen treatment was compared with that following inducible expression of c-Myc or c-Zip (a deletion mutant of c-Myc that lacks the N-terminal transactivation domains) in clonal MCF-7 cell lines. Keywords: Single time point
Project description:Estrogen-responsive genes were identified by transcript profiling of estrogen-treated MCF-7 breast cancer cells. The gene expression profile generated after estrogen treatment was compared with that following inducible expression of c-Myc or c-Zip (a deletion mutant of c-Myc that lacks the N-terminal transactivation domains) in clonal MCF-7 cell lines. Experiment Overall Design: RNA was collected in three independent experiments, each including parental MCF-7 cells treated with 17b-estradiol (E2) or ethanol (EtOH), zinc-treated p-delta-MT-c-Myc cells, zinc-treated p-delta-MT-c-Zip cells and zinc-treated empty vector (p-delta-MT) cells. Cells were arrested for 48 h with 10 nM ICI 182780 and then treated for 6 h with either 100 nM E2 or ethanol vehicle, or 75 mM zinc for the stably transfected cell lines.
Project description:To examine the role of PSF and NONO in estrogen-dependent breast cancer, MCF-7 cells were treated with siRNA targeting PSF, NONO or control siRNA (siControl). Microarray analysis revealed PSF- or NONO-regulated genes in MCF-7 cells.
Project description:To understand the regulatory landscape of oncogene c-Myc in breast cancer, two epigenetic hallmarks of open chromatin, consisting of H3K4me1 and H3K27ac, were investigated by ChIP-seq in distinct types of human breast cancer cells (estrogen receptor positive MCF-7 and triple-negative MDA-MB-231), respectively. By visualizing the ChIP-seq at c-Myc locus, we noticed that the H3K4me1 and H3K27ac signals were enriched remarkably upstream ~65 kb of c-Myc in MCF-7 cells but not in MDA-MB-231 cells. The results indicated that c-Myc may be regulted by an enhancer located upstream ~65 kb.
Project description:Estrogen deprivation using aromatase inhibitors is currently the standard of care for patients with estrogen-receptor (ER)-positive breast cancer. Unfortunately, prolonged estrogen deprivation leads to drug resistance (i.e. hormone-independent growth). We therefore used DNA microarray analysis to study the gene expression profiles of wild-type MCF-7 cells (which are sensitive to antihormone therapy) and long-term estrogen deprived MCF-7:5C and MCF-7:2A breast cancer cells (which are resistance to estrogen-deprivation; aromatase inhibitor resistant). Transcriptional profiling of wild-type MCF-7 cells and estrogen deprived MCF-7:5C and MCF-7:2A cells was performed using Affymetrix Human Genome U133 Plus 2.0 Array. Keywords: breast cancer cells, estrogen