Project description:This SuperSeries is composed of the following subset Series: GSE13858: Global survey of miRNA microarray of uterus, ovariectomized female mice with or without estrogen (E2) treatment GSE13859: Global survey of miRNA microarray of whole embryo, wild type vs estrogen receptor alpha knockout mice Refer to individual Series
Project description:To examine the effect of E2 treatment for the miRNA expression in human MCF-7 cells, MCF-7 cells were treated with or without E2 (100 nM) for 4 hr or 24 hr.
Project description:We generated DNA microarray based gene expression profiles from three estrogen receptor a (ERa) positive breast cancer cell lines stimulated by 17Ã?-estradiol (E2) in vitro over a time course, as well as from MCF-7 cells grown as xenografts in ovariectomized athymic nude mice with E2 supplementation and after its withdrawal. Experiment Overall Design: 8 MCF-7 xenograft profiles (4 with E2,4 without E2), 14 T47D profiles (with E2 treatment in culture from 0 to 24 hr), 10 BT-474 profiles (with E2 treatment from 0 to 24 hr), 12 MCf-7 profiles (with E2 treatment from 0 to 24 hr)
Project description:To examine the effect of E2 treatment for the miRNA expression in human MCF-7 cells, MCF-7 cells were treated with or without E2 (100 nM) for 4 hr or 24 hr. Four group experiments; E2 (100 nM) treatment for 4 hr (MCF-7 E2 4h_1, MCF-7 E2 4h_2), vehicle (ethanol) treatment for 4 hr as Mock control (MCF-7 Mock1, MCF-7 Mock2), E2 (100 nM) treatment for 24 hr (MCF-7 E2 24h_1, MCF-7 E2 24h_2, MCF-7 E2 24h_3), vehicle treatment for 24 hr as Mock control (MCF-7 Mock_3, MCF-7 Mock_4, MCF-7 Mock_5).
Project description:We have evaluated the effects of estrogen over SOX2 expression by maintaining MCF-7 under three distinct conditions: estrogen deprivation for a year (LT -E2 MCF-7), treating MCF-7 cells with estrogen for 48 hours (48hr +E2 MCF-7), and maintaining cells under estrogenic conditions for a year (LT +E2 MCF-7).
Project description:Altered expression of microRNAs (miRNAs), an abundant class of small non-protein-coding RNAs that mostly function as negative regulators of protein-coding gene expression, is common in cancer. Here we analyze the regulation of miRNA expression in response to estrogen, a steroid hormone that is involved in the development and progression of breast carcinomas and that is acting via the estrogen receptors (ER) transcription factors. We set out to thoroughly describe miRNA expression, by using miRNA microarrays and real time RTPCR experiments, in various breast tumor cell lines in which estrogen signaling has been induced by 17β-estradiol (E2). We show that the expression of a broad set of miRNAs decreases following E2 treatment in an ER-dependent manner. We further show that enforced expression of several of the repressed miRNAs reduces E2-dependent cell growth, thus linking expression of specific miRNAs with estrogen-dependent cellular response. In addition, a transcriptome analysis revealed that the E2-repressed miR-26a and miR-181a regulate many genes associated with cell growth and proliferation, including the progesterone receptor gene, a key actor in estrogen signaling. Strikingly, miRNA expression is also regulated in breast cancers of women who had received antiestrogen neoadjuvant therapy thereby showing an estrogen-dependent in vivo regulation of miRNA expression. Overall, our data indicates that the extensive alterations in miRNA regulation upon estrogen signalling pathway plays a key role in estrogen-dependent functions and highlights the utility of considering miRNA expression in the understanding of antiestrogen resistance of breast cancer. 9 samples analyzed. Triplicates were done. MCF-7+miR26a+E2 (n=1 to 3) ; MCF7+miRctrl+E2 (n=1 to 3) ; MCF7+miRctrl+vehicle (n=1 to 3). We generated pairwise comparisons using EASANA from GenoSplice technology: MCF-7+miR26a+E2 versus MCF7+miRctrl+E2 and MCF-7+miRctrl+E2 versus MCF7+miRctrl+vehicle. Fold change ≥1.5 were selected.
Project description:A series of MCF-7 variants were previously developed that are either estrogen-dependent for growth (MCF-7:WS8 cells), or resistant to estrogen deprivation and refractory (MCF-7:2A) or sensitive (MCF-7:5C) to E2-induced apoptosis. To identify genes associated with E2-induced apoptosis, estrogen deprivation-resistant/apoptotic-sensitive 5C cells were compared to both estrogen-dependent MCF-7:WS8 and estrogen deprivation/apoptotic-refractory MCF-7:2A cells
Project description:A series of MCF-7 variants were previously developed that are estrogen-dependent for growth (MCF-7:WS8 cells), or resistant to estrogen deprivation/vulnerable to fast (MCF-7:5C) and delayed (MCF-7:2A) E2-inducible apoptosis. To identify miRNAs associated with aromatase inhibitor (AI)-resistance and vulnerability to E2-induced apoptosis, estrogen deprivation-resistant 5C and 2A cells were compared to estrogen-dependent WS8 cells and among each other.
Project description:Tamoxifen is an anti-estrogen drug used in the treatment of Estrogen Receptor (ER) positive breast cancer. Effects and side effects of tamoxifen is the sum of tamoxifen and all its metabolites. Using concentrations that mimic the clinical situation we examined effects of 4OHtam, 4OHNDtam and NDtam on global gene expression in 17beta-estradiol (E2) treated MCF-7 cells.
