Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA315500 | ENA |
REPOSITORIES: ENA
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Project description:Estrogen deprivation using aromatase inhibitors is currently the standard of care for patients with estrogen-receptor (ER)-positive breast cancer. Unfortunately, prolonged estrogen deprivation leads to drug resistance (i.e. hormone-independent growth). We therefore used DNA microarray analysis to study the gene expression profiles of wild-type MCF-7 cells (which are sensitive to antihormone therapy) and long-term estrogen deprived MCF-7:5C and MCF-7:2A breast cancer cells (which are resistance to estrogen-deprivation; aromatase inhibitor resistant). Transcriptional profiling of wild-type MCF-7 cells and estrogen deprived MCF-7:5C and MCF-7:2A cells was performed using Affymetrix Human Genome U133 Plus 2.0 Array. Keywords: breast cancer cells, estrogen
2008-03-19 | GSE10879 | GEO
Project description:To explore the mechanism of endocrine resistance development in estrogen receptor positive breast cancer, transcriptome analysis of MCF-7 and its endocrine resistant derivatives, including tamoxifen resistant (TAMR) sub-lines and long-term estrogen deprivation (LTED) sub-lines, were performed using microarray.
2023-06-14 | GSE234546 | GEO
Project description:Estrogen deprivation using aromatase inhibitors is currently the standard of care for patients with estrogen-receptor (ER)-positive breast cancer. Unfortunately, prolonged estrogen deprivation leads to drug resistance (i.e. hormone-independent growth). We therefore used DNA microarray analysis to study the gene expression profiles of wild-type MCF-7 cells (which are sensitive to antihormone therapy) and long-term estrogen deprived MCF-7:5C and MCF-7:2A breast cancer cells (which are resistance to estrogen-deprivation; aromatase inhibitor resistant). Transcriptional profiling of wild-type MCF-7 cells and estrogen deprived MCF-7:5C and MCF-7:2A cells was performed using Affymetrix Human Genome U133 Plus 2.0 Array. Experiment Overall Design: We wanted to study the gene expression profiles of the different cell lines in their growth media without any drug treatment. Therefore, MCF-7, MCF-7:5C, and MCF-7:2A cells were grown in estrogen-free media (phenol red-free RPMI medium supplemented with 10% 4X dextran-coated charcoal-treated fetal bovine serum) until they were 70-80% confluent then RNA was extracted, labeled, and hybridized to the Affymetrix Human Genome U133 Plus 2.0 Arrays.
2008-04-05 | E-GEOD-10879 | biostudies-arrayexpress
Project description:MCF-7:5C and MCF-7:2A are two in vitro models of Estrogen Receptor alpha positive (ER+) estrogen deprivation-resistant breast cancer. Both cell lines grow robustly in the absence of estrogen [PMID:1301400, PMID:7780972]. MCF-7:PF is an in vitro model of antihormone resistant breast cancer that exhibits the characteristics of acquired tamoxifen resistance [PMID:24183378] The goal of this study was to compare basal levels of gene expression during exponential phase of growth in MCF-7-derived models of endocrine resistance, relative to their isogenic parental cells
2014-11-30 | GSE60079 | GEO
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
2011-11-21 | GSE29917 | GEO
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.
2017-03-01 | GSE79326 | GEO
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 Each cell line was treated with 10-9 M E2 or vehicle control over a 96 h time course consisting of 7 time points (2, 6, 12, 24, 48, 72 and 96 h) using 6 biological replicates per condition. cRNA probes from individual E2-treated samples were competitively hybridized against time-matched pooled control probes using 2-color Agilent 4x44k human oligonucleotide microarrays.
2011-11-21 | E-GEOD-29917 | biostudies-arrayexpress
Project description:Tamoxifen is an effective anti-estrogen treatment for patients with estrogen receptor-positive (ER+) breast cancer. However, about 30% of such patients receiving tamoxifen as an adjuvant therapy experience recurrence within 15 years, and most patients with advanced disease eventually develop resistance to tamoxifen. To elucidate the underlying molecular mechanisms of tamoxifen resistance, we performed a systematic analysis of miRNA-mediated gene regulation in three clinically-relevant tamoxifen-resistant human breast cancer cell lines (TamRs) compared to their parental tamoxifen-sensitive MCF-7/S0.5 cell line. Alterations in the expression of 131 miRNAs in tamoxifen-resistant vs. parental cell lines were identified, 22 of which were common to all TamRs using both sequencing and LNA-based quantitative PCR technologies. ER+ and tamoxifen sensitive breast cancer cell line (MCF-7/S0.5) and its derived tamoxifen resistant clones: TAMR-1, TAMR-4 and TAMR-8 were miRNA expression profiled in triplicates of each using Exiqon's miRCURY LNA based microRNA Ready-to-use PCR, Human panel I+II, V2.R (Exiqon, product number 203608).
2015-08-01 | E-GEOD-56411 | biostudies-arrayexpress
Project description:Resistance to endocrine therapy agents has presented a clinical obstacle in the treatment of hormone-dependent breast cancer. Our laboratory has initiated a study of microRNA regulation of signaling pathways that may result in breast cancer progression on aromatase inhibitors (AI). Microarray analysis of microRNA expression identified 115 significantly regulated microRNAs, of which 49 microRNAs were believed to be hormone-responsive. Within the AI-resistant cells, microRNAs were differentially expressed between the steroidal and non-steroidal AI-resistant lines. Also, a group of microRNAs were inversely expressed in the AI-resistant lines versus LTEDaro and tamoxifen-resistant. We focused our work on hsa-miR-128a which was hormone-responsive and up-regulated in the letrozole-resistant cell lines. Human miR-128a was shown to negatively target TGFBRI protein expression by binding to the 3âUTR region of the gene. Loss of TGFBRI resulted in compromised sensitivity to the growth inhibitory effects of TGFB in the letrozole-resistant lines. Inhibition of endogenous miR-128a resulted in re-sensitization of the letrozole-resistant lines to TGFB growth inhibitory effects. This data suggests that the hormone-responsive miR-128a can modulate TGFB signaling and survival of the letrozole-resistant cell lines. To our knowledge, this is the first study to address the role of microRNA regulation as well as TGFB signaling in AI-resistant breast cancer cell lines. We believe that in addition to estrogen-modulation of gene expression, hormone-regulated microRNAs may provide an additional level of post-transcriptional regulation of signaling pathways critically involved in breast cancer progression and AI-resistance. To look at microRNA expression profiles of breast cancer cell lines derived from MCF-7 cells that are resistant to endocrine therapy agents. MCF-7 cells that overexpress aromatase (MCF-7aro) were cultured long-term in the presence of endocrine therapy agents until cells acquired resistance. Three different aromatase inhibitors (letrozole, anastrozole or exemestane) were used, as well as the ER antagonist tamoxifen, or the hormone-free long-term estrogen deprived cells (LTED). Three replicates of the control cells (MCF-7aro) and all resistant cells were used for microarray experiments. Total of 23 samples were analyzed by microarray.
2010-05-16 | E-GEOD-17775 | biostudies-arrayexpress
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.
2009-08-04 | E-GEOD-17460 | biostudies-arrayexpress