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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Chang Edmund

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

REPOSITORIES: biostudies-other

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Expression data from human breast cancer cells (MCF-7) coexpressing ERalpha and Erbeta, treated with phytoestrogens

2008-02-07 | GSE9936 | GEO

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.

2008-04-10 | E-GEOD-9936 | biostudies-arrayexpress

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

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.

| S-ECPF-GEOD-4025 | biostudies-other

Transcription profiling of human breast cancer cells expressing ERalpha and treated with 17beta-estradiol

Project description:Gene expression changes caused by estrogen treatment of breast cancer cells that re-express ERalpha was investigated by infecting ER-negative MDA-MB-231 breast cancer cells for 24 h with recombinant adenovirus encoding full-length human ERalpha (Ad-ERalpha) or control vector (Ad-LacZ), and treating them with 0·01% ethanol (vehicle control) or 10-8 M 17beta-estradiol (E2). After 48 h of treatment, total RNA was isolated and used for transcript profiling on Affymetrix GeneChips. Three independent biological replicates of this experiment were carried out.

| S-ECPF-GEOD-2251 | biostudies-other

Transcription profiling of MCF-7 Human Breast Cancer Cells

Project description:SOX genes encode a family of high-mobility group transcription factors that play critical roles in organogenesis. Virtually all members of SOX family have been found to be deregulated in tumors of various origins. However, little is known about the cellular and molecular behaviours involved in the oncogenic potential of SOX proteins. Cell culture experiments, tissue analysis, and molecular profiling revealed that SOX2 promotes cell proliferation and tumorigenesis through its transcription regulation of cell cycle related genes in breast cancer cells Experiment Overall Design: To delineate the molecular mechanism underlying the cell proliferation and tumorigenic properties of SOX2, we investigated the gene expression profile in MCF-7 cells. Briefly, MCF-7 cells were transfected with pcDNA3.1 and Human SOX2 expression constructs respectively. 24 hours after transfection, total RNA collected from control and SOX2-overexpressing MCF-7 cells was used to probe Human Genome GeneChip array U133 Plus 2.0

| S-ECPF-GEOD-11330 | 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 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 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 of human MCF-7 breast cancer cells - glycodelin-induced changes

Project description:Recent reports suggest that glycodelin induces epithelial differentiation. Little is known about the mechanisms involved in this process. To elucidate this we transfected glycodelin-negative MCF-7 breast cancer cells with glycodelin cDNA. Cells transfected with a vector in which glycodelin cDNA was in antisense orientation were used as non-glycodelin-producing controls. Oligo microarray was performed to study gene expression changes between glycodelin-transfected and control cells. Experiment Overall Design: Gene expression differences between MCF-7 breast cancer cells transfected with glycodelin cDNA and the cells transfected with a vector in which glycodelin cDNA was in antisense orientation were studied by oligo microarray.

| S-ECPF-GEOD-7771 | biostudies-other

Transcription profiling of human HMLER breast cancer cells treated with paclitaxel and salinomycin-treated HMLER breast cancer cells

Project description:Screens for agents that specifically kill epithelial cancer stem cells (CSCs) have not been possible due to the rarity of these cells within tumor cell populations and their relative instability in culture. We describe here an approach to screening for agents with epithelial CSC-specific toxicity. We implemented this method in a chemical screen and discovered compounds showing selective toxicity for breast CSCs. One compound, salinomycin, reduces the proportion of CSCs by >100-fold relative to paclitaxel, a commonly used breast cancer chemotherapeutic drug. Treatment of mice with salinomycin inhibits mammary tumor growth in vivo and induces increased epithelial differentiation of tumor cells. In addition, global gene expression analyses show that salinomycin treatment results in the loss of expression of breast CSC genes previously identified by analyses of breast tissues isolated directly from patients. This study demonstrates the ability to identify agents with specific toxicity for epithelial CSCs Experiment Overall Design: Experimentally transformed HMLER breast cancer cells were treated in culture with either paclitaxel (10nM) or salinomycin (1uM) for one week. There were three biologic replicates for each treatment condition.

| S-ECPF-GEOD-17215 | biostudies-other

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