Project description:To investigate global transcriptomics of human MDA-MB-453 breast cancer cells in response to the TDO2/IDO dual inhibitor AT0174 treatment in compared with the vehicle control
Project description:This SuperSeries is composed of the following subset Series: GSE28305: Effect of 5a-dihydrotestosterone on breast cancer cell line MDA-MB-453 GSE28788: Androgen receptor cistrome in breast cancer cell line MDA-MB-453 with 5a-dihydrotestosterone (DHT) stimulation Refer to individual Series
Project description:Androgen receptor (AR) is expressed in 60-70% of breast cancers independent of estrogen receptor (ER) expression, however its function in breast cancer is largely unknown. Our study identified the high level of AR in ERâ??/HER2+ breast tumors and andorgen and AR greatly stimulated growth of MDA-MB-453 breast cancer cells. To define the genome-wide AR binding sites, we performed AR ChIP-seq using MDA-MB-453 breast cancer cells followig stimulation of DHT. We also identified FOXA1 is a crucial AR cofactor in MDA-MB-453 cells and the FOXA cistrome showed signaficant overlap with AR at both early and late time points of DHT stimulation. AR ChIP was performed in MDA-MB-453 breast cancer cells following 5a-dihydrotestosterone (DHT) stimulation for 4h and 16h respectively. FOXA1 ChIP-seq was performed after 4h DHT stimulation in MDA-MB-453 cells.
Project description:Analysis of MDA-MB-453 breast cancer cells treated with the androgen 5a-dihydrotestosterone (DHT) for 6h, 16h and 48h to define the genes that are differentially regulated in response to DHT. MDA-MB-453 breast cancer cells were treated with 5a-dihydrotestosterone (DHT) for time course, followed by RNA extraction and hybridization on Affymetrix microarrays, in order to obtain the gene expression profiles at three time points. The vehicle treated samples are used as control.
Project description:Androgen receptor (AR) is expressed in 60-70% of breast cancers independent of estrogen receptor (ER) expression, however its function in breast cancer is largely unknown. Our study identified the high level of AR in ERâ/HER2+ breast tumors and andorgen and AR greatly stimulated growth of MDA-MB-453 breast cancer cells. To define the genome-wide AR binding sites, we performed AR ChIP-seq using MDA-MB-453 breast cancer cells followig stimulation of DHT. We also identified FOXA1 is a crucial AR cofactor in MDA-MB-453 cells and the FOXA cistrome showed signaficant overlap with AR at both early and late time points of DHT stimulation.
Project description:The effect of transient transfection of a construct designed to over-express the androgen receptor (AR) variant AR-V7 on gene expression in MDA-MB-453 cells was assessed using Affymetrix Gene 2.0 ST arrays. Transfection of an AR-expressing construct or an empty construct served as controls. AR-V7, AR or empty vector was transfected into MDA-MB-453 cells. Cells were treated with vehicle control or DHT.
Project description:Analysis of MDA-MB-453 breast cancer cells treated with the androgen 5a-dihydrotestosterone (DHT) for 6h, 16h and 48h to define the genes that are differentially regulated in response to DHT.
Project description:This study aimed to identify differential expressed genes before and after treatment with the compound sulforaphene, using the MDA-MB-453 breast cancer cell line as a model.
Project description:The effect of transient transfection of a construct designed to over-express the androgen receptor (AR) variant AR-V7 on gene expression in MDA-MB-453 cells was assessed using Affymetrix Gene 2.0 ST arrays. Transfection of an AR-expressing construct or an empty construct served as controls.