Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

56 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Amplitude modulation of androgen signaling by c-MYC [RNA-Seq]

ABSTRACT: Androgen-stimulated growth of the molecular apocrine breast cancer is mediated by an androgen receptor (AR)-regulated transcriptional program. Through profiling the genomic licalizations of AR and its co-regulators FOXA1 and TCF7L2 in MDA-MB-453 breast cancer cells, we revealed the molecular details of the AR-centered regulatory network. We further identified that c-MYC is a key downstream target co-regulated by AR, FOXA1 and TCF7L2, and reinforces the transctiopnal activation of androgen-responsive genes in this subtype of breast cancers. MDA-MB-453 breast cancer cells were transfected with control of MYC siRNA for 48 h, followed by treatment with 10nM DHT or vehicle for 6 h. The cells were subjected to mRNA purification and library praparation for RNA-seq on Illumina HiSeq2000 platform.

ORGANISM(S): Homo sapiens

SUBMITTER: Yiwen Chen

PROVIDER: E-GEOD-45202 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Amplitude modulation of androgen signaling by c-MYC [ChIP-Seq]

Project description:Androgen-stimulated growth of the molecular apocrine breast cancer is mediated by an androgen receptor (AR)-regulated transcriptional program. Through profiling the genomic licalizations of AR and its co-regulators FOXA1 and TCF7L2 in MDA-MB-453 breast cancer cells, we revealed the molecular details of the AR-centered regulatory network. We further identified that c-MYC is a key downstream target co-regulated by AR, FOXA1 and TCF7L2, and reinforces the transctiopnal activation of androgen-responsive genes in this subtype of breast cancers. AR and FOXA1 ChIP-seq were performed in MDA-MB-453 breast cancer cells with treatment of 5a-dihydrotestosterone (DHT) for 16 h. TCF7L2 ChIP-seq was performed in MDA-MB-453 cells treated with vehicle or DHT for 16 h, respectively. MYC ChIP-seq was performed in MDA-MB-453 cells following 6 h DHT stimulation.

2013-03-16 | E-GEOD-45201 | biostudies-arrayexpress

Androgen receptor cistrome in breast cancer cell line MDA-MB-453 with 5a-dihydrotestosterone (DHT) stimulation

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.

2011-07-11 | E-GEOD-28788 | biostudies-arrayexpress

Effect of FOXA1 over-expression upon AR binding in AR-driven cancers

Project description:We performed androgen receptor (AR) ChIP-seq after GFP control or FOXA1 over-expression in two AR driven cancer models; LNCaP prostate cancer cell line and MDA-MB-453 molecular apocrine breast cancer cell line.

2014-01-14 | E-MTAB-1749 | biostudies-arrayexpress

ChIP-seq study using a cell line model of ER_ AR+ molecular apocrine tumours (AR_FoxA1_molecular_apocrine)

Project description:Breast cancer is a heterogeneous disease and several distinct subtypes exist based on differential gene expression patterns. Molecular apocrine tumours were recently identified as an additional subgroup, characterised as oestrogen receptor negative and androgen receptor positive (ER_ AR+), but with an expression profile resembling ER+ luminal breast cancer. One possible explanation for the apparent incongruity is that ER gene expression programmes could be recapitulated by AR. Using a cell line model of ER_ AR+ molecular apocrine tumours (termed MDA-MB-453 cells), we map global AR binding events and find a binding profile that is similar to ER binding in breast cancer cells. We find that AR binding is a near-perfect subset of FoxA1 binding regions, a level of concordance never previously seen with a nuclear receptor. AR functionality is dependent on FoxA1, since silencing of FoxA1 inhibits AR binding, expression of the majority of the molecular apocrine gene signature and growth cell growth. These findings show that AR binds and regulates ER cis-regulatory elements in molecular apocrine tumours, resulting in a transcriptional programme reminiscent of ER-mediated transcription in luminal breast cancers.

2012-02-18 | E-MTAB-986 | biostudies-arrayexpress

Breast cancer cell line MDA-MB-453 response to DHT

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

2011-07-10 | E-GEOD-28789 | biostudies-arrayexpress

Effect of over-expression of AR-V7 in MDA-MB-453 breast cancer cells

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.

2015-02-10 | E-GEOD-65738 | biostudies-arrayexpress

Exploration of the redundancy between FOXA1 and AP2alpha in androgen receptor transcription complex

Project description:We performed a comparision of AR binding sites as well as the histone modifications H3K27 acetylation and H3K4 monomethylation in the presence and absence of FoxA1 in the molecular apocrine breast cancer cell line, MDA-MB-453. We also probed AP2alpha binding in asynchronous MDA-MB-453 cells.

2014-04-17 | E-MTAB-1694 | biostudies-arrayexpress

Effect of 5a-dihydrotestosterone on breast cancer cell line MDA-MB-453

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.

2011-07-11 | E-GEOD-28305 | biostudies-arrayexpress

Amplitude modulation of androgen signaling by c-MYC [RNA-Seq]

2013-03-16 | GSE45202 | GEO

Amplitude modulation of androgen signaling by c-MYC [ChIP-Seq]

2013-03-16 | GSE45201 | GEO