Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling by array of human MCF-7 breast cancer cells treated with tamoxifen or adenovirus expressing ERbeta

ABSTRACT: The beneficial effect of the selective estrogen receptor (ER) modulator tamoxifen in the treatment and prevention of breast cancer is assumed to be through its ability to antagonize the stimulatory actions of estrogen, although tamoxifen can also have some estrogen-like agonist effects. Here, we report that, in addition to these mixed agonist/antagonist actions, tamoxifen can also selectively regulate a unique set of >60 genes, which are minimally regulated by estradiol (E2) or raloxifene in ERalpha-positive MCF-7 human breast cancer cells. This gene regulation by tamoxifen is mediated by ERalpha and reversed by E2 or ICI 182,780. Introduction of ERbeta into MCF-7 cells reverses tamoxifen action on approximately 75% of these genes. To examine whether these genes might serve as markers of tamoxifen sensitivity and/or the development of resistance, their expression level was examined in breast cancers of women who had received adjuvant therapy with tamoxifen. High expression of two of the tamoxifen-stimulated genes, YWHAZ/14-3-3z and LOC441453, was found to correlate significantly with disease recurrence following tamoxifen treatment in women with ER-positive cancers and hence seem to be markers of a poor prognosis. Our data indicate a new dimension in tamoxifen action, involving gene expression regulation that is tamoxifen preferential, and identify genes that might serve as markers of tumor responsiveness or resistance to tamoxifen therapy. This may have a potential effect on the choice of tamoxifen versus aromatase inhibitors as adjuvant endocrine therapy.

ORGANISM(S): Homo sapiens

SUBMITTER: Frasor J

PROVIDER: S-ECPF-GEOD-4025 | biostudies-other | 2006 Jul

REPOSITORIES: biostudies-other

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling of human breast cancer cells (MCF-7) coexpressing ERalpha and Erbeta, treated with phytoestrogens

Project description:We used microarrays to detail the global transcriptional response mediated by ERalpha or ERbeta to the phytoestrogen genistein in the MCF-7 human breast cancer cell model. Experiment Overall Design: MCF-7 human breast cancer cells expressing endogenouse Estrogen Receptor Alpha (ERalpha) were infected with adenovirus carrying either estrogen receptor beta (AdERb) or no insert (Ad) at multiplicity of infection (moi) of 20. Cells were then treated with either vehicle control (veh), 6nM 17beta-estradiol (E2), 6nM genistein (LG), 300nM genistein (HG), 300nM S-Equol (EQ), HG+3uM ICI182,780 (IG), EQ+3uM ICI 182,780(IE) for a additional periods of 4h or 24hr before RNA extraction and hybridization on Affymetrix microarrays. We sought to determine if genistein and S-Equol, phytoestrogens selective for the ERbeta can elicit transcriptional response distinctive from those mediated by the ERalpha.

| S-ECPF-GEOD-9936 | biostudies-other

Transcription profiling by array of human breast cancer MCF-7 cells treated with 17-AAG

Project description:17-AAG treatment of MCF-7 Microarray Files containing additional statistical analysis and data for meta-probesets are available on the FTP site for the experiment, in E-MTAB-339.additional.zip

| S-ECPF-MTAB-339 | biostudies-other

Transcription profiling by array of human breast cancer cell line MCF-7 treated with estradiol

Project description:The Estrogen Receptor cofactors SRC1 (NCOA1, KAT13A), SRC2 (NCOA2, GRIP1, TIF2, KAT13C) , SRC3 (NCOA3, AIB1, KAT13B, Rac3) , CBP and p300 are assessed for their genome-wide chromatin binding capacities in the breast cancer cell line MCF7. To determine the Estrogen Receptor dependency of interactions, experiments were performed in the absence of hormone and after Estradiol treatment. In addition, the data were compared with Estrogen Receptor ChIP-seq data from the same timepoint of Estradiol treatment.

| S-ECPF-MTAB-788 | biostudies-other

Transcription profiling by array of human MCF cells treated with estrogen

Project description:The estrogen receptor is the master transcriptional regulator of breast cancer phenotype and the archetype of a molecular therapeutic target. We mapped all estrogen receptor and RNA polymerase II binding sites on a genome-wide scale, identifying the authentic cis binding sites and target genes, in breast cancer cells. Combining this unique resource with gene expression data demonstrates distinct temporal mechanisms of estrogen-mediated gene regulation,particularly in the case of estrogen-suppressed genes. Furthermore, this resource has allowed the identification of cis-regulatory sites in previously unexplored regions of the genome and the cooperating transcription factors underlying estrogen signaling in breast cancer. Experiment Overall Design: This Series currently contains the gene expression data accompaning Carroll JS et al. Nature Genetics 38,1289-1297(2006). MCF7 cells were stimulated with 100 nM estrogen for 0, 3, 6, or 12h. All experiments were performed in triplicate.

| S-ECPF-GEOD-11324 | biostudies-other

Transcription profiling by array of human MCF-7 breast cancer cells

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.

| S-ECPF-GEOD-11791 | biostudies-other

Transcription profiling by array of human breast cancers after treatment with tamoxifen

Project description:Purpose: A number of microarray studies have reported distinct molecular profiles of breast cancers (BC): basal-like, ErbB2-like and two to three luminal-like subtypes. These were associated with different clinical outcomes. However, although the basal and the ErbB2 subtypes are repeatedly recognized, identification of estrogen receptor (ER)-positive subtypes has been inconsistent. Refinement of their molecular definition is therefore needed. Materials and methods: We have previously reported a gene-expression grade index (GGI) which defines histological grade based on gene expression profiles. Using this algorithm, we assigned ER-positive BC to either high or low genomic grade subgroups and compared these to previously reported ER-positive molecular classifications. As further validation, we classified 666 ER-positive samples into subtypes and assessed their clinical outcome. Results: Two ER-positive molecular subgroups (high and low genomic grade) could be defined using the GGI. Despite tracking a single biological pathway, these were highly comparable to the previously described luminal A and B classification and significantly correlated to the risk groups produced using the 21-gene recurrence score. The two subtypes were associated with statistically distinct clinical outcome in both systemically untreated and tamoxifen-treated populations. Conclusions: The use of genomic grade can identify two clinically distinct ER-positive molecular subtypes in a simple and highly reproducible manner across multiple datasets. This study emphasizes the important role of proliferation-related genes in predicting prognosis in ER-positive BC. Experiment Overall Design: dataset of microarray experiments from primary breast tumors used to assess the reationship between GGI, molecular subtypes, and tamoxifen resistance. Experiment Overall Design: No replicate, no reference sample.

| S-ECPF-GEOD-6532 | biostudies-other

Transcription profiling by array of MCF-7 and MDA-MB-213 cells treated with docetaxel

Project description:Two breast cancer cell lines, MCF-7 and MDA-MB-213, were treated progressively with docetaxel.

| S-ECPF-MEXP-3982 | biostudies-other

Transcription profiling by array of human MDA-MB-231 cells with adenovirus-expressed estradiol-ERalpha, estradiol-ERbeta, and ERE-binding defective mutants

Project description:This SuperSeries is composed of the following subset Series:; GSE9757: Response to estradiol-ERalpha; GSE9758: Response to estradiol-ERalpha ERE Binding defective mutant; GSE9759: Response to estradiol-Erbeta and estradiol-ERbeta ERE binding defective mutant Experiment Overall Design: Refer to individual Series

| S-ECPF-GEOD-9761 | biostudies-other

Transcription profiling by array of breast cancer samples treated and non-treated with celecoxib

Project description:Biopsies and surgical specimens were obtained from breast tumours treated and non-treated with celecoxib 400mg twice daily for 2 weeks

| S-ECPF-MTAB-566 | biostudies-other

Transcription profiling of human MCF-7 breast cancer cell line transfected with adenovirus expressing Erbeta treated with estrogen or tamoxifen reveals tamoxifen can selectively regulate a unique set of >60 genes, which are minimally regulated by estradiol (E2) or raloxifene.

Project description:The beneficial effect of the selective estrogen receptor (ER) modulator tamoxifen in the treatment and prevention of breast cancer is assumed to be through its ability to antagonize the stimulatory actions of estrogen, although tamoxifen can also have some estrogen-like agonist effects. Here, we report that, in addition to these mixed agonist/antagonist actions, tamoxifen can also selectively regulate a unique set of >60 genes, which are minimally regulated by estradiol (E2) or raloxifene in ERalpha-positive MCF-7 human breast cancer cells. This gene regulation by tamoxifen is mediated by ERalpha and reversed by E2 or ICI 182,780. Introduction of ERbeta into MCF-7 cells reverses tamoxifen action on approximately 75% of these genes. To examine whether these genes might serve as markers of tamoxifen sensitivity and/or the development of resistance, their expression level was examined in breast cancers of women who had received adjuvant therapy with tamoxifen. High expression of two of the tamoxifen-stimulated genes, YWHAZ/14-3-3z and LOC441453, was found to correlate significantly with disease recurrence following tamoxifen treatment in women with ER-positive cancers and hence seem to be markers of a poor prognosis. Our data indicate a new dimension in tamoxifen action, involving gene expression regulation that is tamoxifen preferential, and identify genes that might serve as markers of tumor responsiveness or resistance to tamoxifen therapy. This may have a potential effect on the choice of tamoxifen versus aromatase inhibitors as adjuvant endocrine therapy.

2007-10-02 | E-GEOD-4025 | 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