ERα gene expression profile in MCF7 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Anne Katchy
PROVIDER: E-GEOD-45557 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Comparison of the basal and estrogen-induced effects on genome-wide transcription in ERM-NM-1-positive breast cancer cell lines T47D and MCF7 after lentiviral transduction with ERM-NM-2. Comparison of ERM-NM-2-transduced T47D and MCF7 cells versus respective control-transduced cells, in the presence of vehicle or estrogen. Each comparison in technical and biological duplicate.
2013-11-21 | E-GEOD-45047 | biostudies-arrayexpress
Project description:The estrogen receptor (ER)M-NM-21 is successively lost during cancer progression, whereas its splice variant, ERM-NM-22, is expressed in advanced prostate cancer. The latter form of cancer often metastasizes to bone, and we wanted to investigate whether the loss of ERM-NM-21 and/or the expression of ERM-NM-22 affect such signaling pathways in prostate cancer. Using PC3 and 22Rv1 prostate cancer cell lines that stably express ERM-NM-21 or ERM-NM-22, we found that the ERM-NM-2 variants differentially regulate genes known to affect tumor behavior. We found that ERM-NM-21 repressed the expression of the bone metastasis regulator Runx2 in PC3 cells. By contrast, RUNX2 expression was up-regulated at the mRNA level by ERM-NM-22 in PC3 cells, whereas Slug was up-regulated by ERM-NM-22 in both PC3 and 22Rv1 cells. In addition, the expression of Twist1, a factor whose expression strongly correlates with high Gleason grade prostate carcinoma, was increased by ERM-NM-22. In agreement with the increased Twist1 expression, we found increased expression of Dickkopf homolog 1; Dickkopf homolog 1 is a factor that has been shown to increase the RANK ligand/osteoprotegerin ratio and enhance osteoclastogenesis, indicating that the expression of ERM-NM-22 can cause osteolytic cancer. Furthermore, we found that only ERM-NM-21 inhibited proliferation, whereas ERM-NM-22 increased proliferation. The expression of the proliferation markers Cyclin E, c-Myc, and p45(Skp2) was differentially affected by ERM-NM-21 and ERM-NM-22 expression. In addition, nuclear M-NM-2-catenin protein and its mRNA levels were reduced by ERM-NM-21 expression. In conclusion, we found that ERM-NM-21 inhibited proliferation and factors known to be involved in bone metastasis, whereas ERM-NM-22 increased proliferation and up-regulated factors involved in bone metastasis. Thus, in prostate cancer cells, ERM-NM-22 has oncogenic abilities that are in strong contrast to the tumor-suppressing effects of ERM-NM-21. The GFP vs. ERbeta1 comparison was carried out with three replicate dye-swaps, six arrays total. The GFP vs. ERbeta2 comparison was carried out with two replicate dye-swaps, four arrays total.
2012-10-03 | E-GEOD-35095 | biostudies-arrayexpress
Project description:Endocrine disrupting chemicals (EDCs) are compounds that disrupt normal hormonal signaling. Examples are Xenoestrogens (e.g BPA) and Phytoestrogens (e.g isoflavones). Comparison of EDC treated versus vehicle treated MCF7 parental cells. Each comparison in technical and biological duplicate.
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Project description:Bisphenol A Exposure and Multiple Sclerosis Risk Comparison of vehicle-treated vs. BPA-treated mouse testes tissue. Each comparison in technical and biological duplicate (Done twice: total 4 replicates)
2013-10-22 | E-GEOD-45917 | biostudies-arrayexpress
Project description:Two subtypes of the estrogen receptor, ERalpha and ERbeta, mediate the actions of estrogens, and the majority of human breast tumors contain both ERalpha and ERbeta. To examine the possible interactions and modulatory effects of ERbeta on ERalpha activity, we have used adenoviral gene delivery to produce human breast cancer (MCF-7) cells expressing ERbeta, along with their endogenous ERalpha. We have examined the effects of ERβ expression on genome-wide gene expression by Affymetrix GeneChip microarrays. We find that ERbeta modulated estrogen gene expression on nearly 24% of E2-stimulated genes but only 8% of E2-inhibited genes. We find that ERbeta modulation is gene-specific, enhancing or counteracting ERalpha regulation for distinct subsets of estrogen target genes. Introduction of ERbeta into ERalpha-containing cells induced up/down-regulation of many estrogen target in the absence of any added ligand. In addition, ERbeta presence elicited the expression of a unique set of genes that were not regulated by ERalpha alone. ERbeta modulated the expression of genes in many functional categories, but the greatest numbers were associated with transcription factor and signal transduction pathways. Regulation of multiple components in the TGF beta, SDF1, and semaphorin pathways, may contribute to the suppression of proliferation observed with ERbeta both in the presence and absence of estrogen. Hence, ERbeta modulates ERalpha gene regulation in diverse ways that may contribute to its growth-inhibiting beneficial effects in breast cancer Keywords: modulatory effects of ERb on ERa
2006-08-10 | GSE4006 | GEO
Project description:Estrogen plays an important role in the regulation of vascular tone and in the pathophysiology of cardiovascular disease. Physiological effects of estrogen are mediated through estrogen receptors alpha (ERalpha) and beta (ERbeta), which are both expressed in vascular smooth muscle and endothelial cells. However, the molecular pathways mediating estrogen effects in blood vessels are not well defined. We have performed gene expression profiling in the mouse aorta to identify comprehensive gene sets the expression of which is regulated by long-term (1 wk) estrogen treatment. The ER subtype dependence of the alterations in gene expression was characterized by parallel gene expression profiling experiments in ERalpha-deficient [ERalpha knockout (ERalphaKO)] and ERbeta-deficient (ERbetaKO) mice. Importantly, these data revealed that ERalpha- and ERbeta-dependent pathways regulate distinct and largely nonoverlapping sets of genes. Whereas ERalpha is essential for most of the estrogen-mediated increase in gene expression in wild-type aortas, ERbeta mediates the large majority of estrogen-mediated decreases in gene expression. Biological functions of the estrogen-regulated genes include extracellular matrix synthesis, in addition to electron transport in the mitochondrion and reactive oxygen species pathways. Of note, the estrogen/ERbeta pathway mediates down-regulation of mRNAs for nuclear-encoded subunits in each of the major complexes of the mitochondrial respiratory chain. Several estrogen-regulated genes also encode transcription factors. Overall, these findings provide a foundation for understanding the molecular basis for estrogen effects on vasculature gene expression. Keywords: estrogen, estrogen receptor knockout, gene expression, mouse aorta
2007-10-19 | GSE9371 | GEO
Project description:Two subtypes of the estrogen receptor, ERalpha and ERbeta, mediate the actions of estrogens, and the majority of human breast tumors contain both ERalpha and ERbeta. To examine the possible interactions and modulatory effects of ERbeta on ERalpha activity, we have used adenoviral gene delivery to produce human breast cancer (MCF-7) cells expressing ERbeta, along with their endogenous ERalpha. We have examined the effects of ERβ expression on genome-wide gene expression by Affymetrix GeneChip microarrays. We find that ERbeta modulated estrogen gene expression on nearly 24% of E2-stimulated genes but only 8% of E2-inhibited genes. We find that ERbeta modulation is gene-specific, enhancing or counteracting ERalpha regulation for distinct subsets of estrogen target genes. Introduction of ERbeta into ERalpha-containing cells induced up/down-regulation of many estrogen target in the absence of any added ligand. In addition, ERbeta presence elicited the expression of a unique set of genes that were not regulated by ERalpha alone. ERbeta modulated the expression of genes in many functional categories, but the greatest numbers were associated with transcription factor and signal transduction pathways. Regulation of multiple components in the TGF beta, SDF1, and semaphorin pathways, may contribute to the suppression of proliferation observed with ERbeta both in the presence and absence of estrogen. Hence, ERbeta modulates ERalpha gene regulation in diverse ways that may contribute to its growth-inhibiting beneficial effects in breast cancer Experiment Overall Design: MCF-7 cells expressing endogenous ERalpha were infected with adenovirus carrying either estrogen receptor beta (AdERb) or no insert (Ad) at multiplicity of infection (moi) of 5 or 50. Cells were infected with adenovirus for a period of 48hr before treatment with ligand (vehicle control or 10nM 17beta-estradiol) for a additional period of 24hr before harvest.
2009-04-24 | E-GEOD-4006 | biostudies-arrayexpress
Project description:Estrogens exert many important effects in bone, a tissue that contains both estrogen receptors alpha and beta (ERalpha and ERbeta). To compare the actions of these receptors, we generated U2OS human osteosarcoma cells stably expressing ERalpha or ERbeta, at levels comparable to those in osteoblasts, and we characterized their response to estradiol (E2) over time using Affymetrix GeneChip microarrays to determine the expression of approximately 12,000 genes, followed by quantitative PCR verification of the regulation of selected genes. Of the ca. 100 regulated genes we identified, some were stimulated by E2 equally through ERalpha and ERbeta, whereas others were selectively stimulated via ERalpha or ERbeta. The E2-regulated genes showed three distinct temporal patterns of expression over the 48 h time course studied. Of the functional categories of the E2-regulated genes, most numerous were those encoding cytokines and factors associated with immune response, signal transduction, and cell migration and cytoskeleton regulation, indicating that E2 can exert effects on multiple pathways in these osteoblast-like cell lines. Of note, E2 up-regulated several genes associated with cell motility selectively via ERbeta, in keeping with the selective E2 enhancement of the motility of ERbeta-containing cells. On genes regulated equally by E2 via ERalpha or ERbeta, the phytoestrogen genistein preferentially stimulated gene expression via ERbeta. These studies indicate both common as well as distinct target genes for these two ERs, and identify many novel genes not previously known to be under estrogen regulation. Keywords: other
2004-04-10 | GSE1153 | GEO
Project description:Purpose: Endocrine therapies, such as tamoxifen are commonly given to most patients with estrogen receptor (ER) alpha-positive breast carcinoma but are not indicated for persons with ERalpha-negative cancer. The factors responsible for response to tamoxifen in 5-10% of patients with ERalpha-negative tumors are not clear. The aim of the present study was to elucidate the biology and role of the second ER, ERbeta, in patients treated with adjuvant tamoxifen. Experimental Design: We investigated ERbeta by immunohistochemistry in 353 stage II primary breast tumors from patients treated with two years adjuvant tamoxifen, and generated gene expression profiles for a representative subset of 88 tumors. Results: ERbeta was associated with increased survival (distant disease-free survival, P=0.01; overall survival, P=0.22), and in particular within ERalpha-negative patients (P=0.003; P=0.04), but not in the ERalpha-positive subgroup (P=0.49; P=0.88). Lack of ERbeta conferred early relapse (hazard ratio, 14; 95% CI, 1.8-106; P=0.01) within the ERalpha-negative subgroup even after adjustment for other markers. ERalpha was an independent marker only within the ERbeta-negative tumors (hazard ratio, 0.44; 95% CI, 0.21-0.89; P=0.02). An ERbeta gene expression profile was identified and was markedly different from the ERalpha signature. Conclusion: Expression of ERbeta is an independent marker for favorable prognosis after adjuvant tamoxifen treatment in ERalpha-negative breast cancer patients, and involves a gene expression program distinct from ERalpha. These results may be highly clinically significant, because in the U.S. alone, approximately 10,000 women are diagnosed annually with ERalpha-negative/ERbeta-positive breast carcinoma and may benefit from adjuvant tamoxifen. Keywords: Disease state analysis
2007-04-01 | GSE6577 | GEO
Project description:This submission is a part of two separate studies: a study of estrogen receptor-alpha (ERalpha)-mediated gene expression in response to different ligands and a study examining the roles of ERalpha and ERbeta in gene regulation in breast cancer cells.
2013-12-01 | GSE45557 | GEO