Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

31 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling by array of aromatase-inhibitor-resistant breast cancer cell lines derived from T-47D

ABSTRACT: To identify the genes which have relation to aromatase-inhibitor-resistance, we compared the gene expression of aromatase-inhibitor-resistant cell, A3, with that of parent cell line, T-47D.

ORGANISM(S): Homo sapiens

SUBMITTER: Rika Fujii

PROVIDER: E-MTAB-1933 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

The gene expression of aromatase-inhibitor-resistant cell line

Project description:To identify the genes which have relation to aromatase-inhibitor-resistance, we compared the gene expression of aromatase-inhibitor-resistant cell, A3, with that of parent cell line, T-47D. Because A3 showed remarkable cell proliferation by 1nM Dihydrotestosterone(DHT), cells were cultured with DHTand bicalutamide for 24h, and total RNA was extracted.

2014-04-01 | E-GEOD-51390 | biostudies-arrayexpress

Investigation of androgen-regulated lncRNAs in prostate cancer cells

Project description:Prostate cancer is the most common cancer in men and androgen receptor (AR) downstream signalings promote prostate cancer cell proliferation. To investigate the AR signaling, we performed directional RNA sequence analysis in AR positive prostate cancer cell line, LNCaP and VCaP. Using Noncode and GENCODE data sets. We identified androgen-regulated long non-coding RNAs (lncRNAs) in prostate cancer cells. Directional RNA sequence analysis of androgen-regulated lncRNAs in prostate cancer cells

2016-08-01 | E-GEOD-82223 | biostudies-arrayexpress

Androgen-induced lncRNA SOCS2-AS1 Promotes Cell Growth and Inhibits Apoptosis in Prostate Cancer Cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-08-01 | E-GEOD-82225 | biostudies-arrayexpress

Expression data from DHT stimulation vs. control in LNCaP cells

Project description:Expression data from DHT stimulation vs. control in LNCaP cells LNCaP cells were maintained in phenol red-free RPMI supplemented with 10% charcoal/dextran stripped FCS for three days before stimulation with 100 nM dihydrotestosterone (DHT) for 48 hours

2010-02-21 | E-GEOD-14988 | biostudies-arrayexpress

MYC regulation of a "poor prognosis" metastatic cancer cell state

Project description:This SuperSeries is composed of the following subset Series: GSE14987: Expression data from ERBB2 over-expression and EGF stimulation in MCF10A cells GSE14988: Expression data from DHT stimulation vs. control in LNCaP cells Refer to individual Series

2010-02-21 | E-GEOD-14990 | biostudies-arrayexpress

Genome-wide analysis of matched microRNA-mRNA time-course data after androgen injection to prostate cancer LNCaP cell line

Project description:Androgen receptor (AR) signalling pathway plays an important role in carcinogenesis and development of prostate cancer. The involvement of microRNA (miRNA) in this process is still largely unknown. In this study, we performed a matched miRNA-mRNA time-course expression profiling to reveal androgen response in hormone-sensitive prostate cancer cells.We introduced novel statistics Response Score (RS) and Modulation Score (MS) to identify significant androgen-regulated target genes and miRNA-modulated target mRNAs. Based on the analysis, we found several novel androgen-regulated targets, which had significant androgen response in expression pattern, and were highly enriched in predicted androgen responsive elements (AREs). AR-bindings to these AREs were validated with ChIP assay. Furthermore, a set of target mRNAs involved in crucial processes of tumor progression were identified to be significantly regulated by these miRNAs. Therefore, a miRNA-mediated androgen signalling network was inferred, including three novel feedback mechanisms for AR self-modulation. In conclusion, our study provides new approaches to further miRNA regulation research and contributes novel findings into miRNA-mediated pathological effects in prostate cancer. Total RNA obtained from androgen dihydrotestosterone (DHT) subjected to LNCaP cells in vitro at 20min, 40min, 1h, 2h, 4h, 8h, 16h, 24h and 48h, compared to the control at 0h.

2011-12-31 | E-GEOD-21245 | biostudies-arrayexpress

Transcription profiling of human prostate cancer cells over-expressing androgen receptor following dihydrotestosterone treament

Project description:dose and time dependent responses of dihydrotestosterone in androgen receptor over-expressing prostate cancer cells.

2009-10-09 | E-MEXP-2286 | 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

Ligand-Dependent Enhancer Activation Regulated by Topoisomerase-I Activity

Project description:The discovery that enhancers are regulated transcription units, encoding eRNAs, has raised new questions about the mechanisms of their activation. Here, we report an unexpected molecular mechanism that underlies ligand-dependent enhancer activation, based on DNA nicking to relieve torsional stress from eRNA synthesis. Using dihydrotestosterone (DHT)-induced binding of androgen receptor (AR) to prostate cancer cell enhancers as a model, we show rapid recruitment, within minutes, of DNA topoisomerase I (TOP1) to a large cohort of AR-regulated enhancers. Furthermore, we show that the DNA nicking activity of TOP1 is a prerequisite for robust eRNA synthesis and enhancer activation and is kinetically accompanied by the recruitment of ATR and the MRN complex, followed by additional components of DNA damage repair machinery to the AR-regulated enhancers. Together, our studies reveal a linkage between eRNA synthesis and ligand-dependent TOP1-mediated nicking - a strategy exerting quantitative effects on eRNA expression in regulating AR-bound enhancer-dependent transcriptional programs. Genome-wide binding analysis of AR, TOP1, MRE11 in prostate cancer cell line LNCaP with or without 5alpha-dihydrotestosterone (DHT) treatment. Nascent RNA analysis by global nuclear run-on (GRO-seq) in LNCaP cells transfected with siRNA with or without DHT treatment. Distribution of transcriptionally engaged RNA Pol II in LNCaP cells with or without DHT treatment by precision nuclear run-on and sequencing (PRO-seq).

2015-01-22 | E-GEOD-63202 | biostudies-arrayexpress

"Drug-seq": An Approach to Identify the Genomic Targets of Chemicals Identified by Functional Phenotypic Screens [Drug-seq]

Project description:Here we report an approach that has permitted us to uncover the sites and mechanisms of action of a drug, referred to as SD70, initially identified by phenotypic screening for inhibitors of ligand and genotoxic stress-induced translocations in prostate cancer cells. Based on synthesis of a derivatized form of SD70 that permits its application for a ChIP-seq-like approach, referred to as Drug-seq, we were next able to efficiently map the genome-wide binding locations of this small molecule, revealing that it largely co-localized with androgen receptor (AR) on regulatory enhancers. Based on these observations, we performed the appropriate global analyses to ascertain that SD70 inhibits the androgen-dependent AR program, and prostate cancer cell growth, acting, at least in part, by functionally inhibiting the jumonji (JMJ) domain-containing demethylase, KDM4C. Drug-seq represents a powerful strategy for new drug development by mapping genome-wide location of small molecules, a powerful adjunct to contemporary drug development strategies. Drug-seq assay followed by high-throughput sequencing (HT-seq).

2014-07-01 | E-GEOD-55901 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data