Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA98897 | ENA |
REPOSITORIES: ENA
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Project description:Pea3 and Erm are transcription factors belonging to the ETS family which are involved in tumorigenesis, particularly mammary oncogenesis. To elucidate the mechanism of Pea3/Erm induced tumorigenesis in mouse mammary cancerous MMT cells (ATCC CCL-51), we have down-regulated Pea3 or Erm expression in this cell line by using small interfering RNA and performed a microarray analysis using Applied Biosystems AB1700 technology to define target associated genes. Keywords: Comparative transcriptome hybridization, small interfering RNA, mouse mammary cancerous cells Mouse mammary cancerous MMT cells (ATCC CCL-51) have been transfected with a siRNA control, an erm-directed siRNA or an pea3-directed siRNA. MMT cells were also used to determine the modifications due to the transfection protocol. These conditions correspond to four sample. Two biological replicate were used for the MMT cells (control sample), three biological replicates were used for the siRNA control (control sample) and erm-directed siRNA (reference sample) MMT cells and four biological replicates were used for the pea3-directed siRNA (reference sample) MMT cells. Transcriptome profiles (28.218 validated mouse genes) were acquired using Applied Biosystems AB1700 technology, which make use of chemiluminescence-based detection chemistry.
2008-08-01 | E-GEOD-6588 | biostudies-arrayexpress
Project description:Pea3 and Erm are transcription factors belonging to the ETS family which are involved in tumorigenesis, particularly mammary oncogenesis. To elucidate the mechanism of Pea3/Erm induced tumorigenesis in mouse mammary cancerous MMT cells (ATCC CCL-51), we have down-regulated Pea3 or Erm expression in this cell line by using small interfering RNA and performed a microarray analysis using Applied Biosystems AB1700 technology to define target associated genes. Keywords: Comparative transcriptome hybridization, small interfering RNA, mouse mammary cancerous cells
2008-08-01 | GSE6588 | GEO
Project description:The initiation of breast cancer is associated with increased expression of tumor-promoting estrogen receptor M-NM-1 (ERM-NM-1) protein and decreased expression of tumor-suppressive ERM-NM-2 protein. However, the mechanism underlying this process is unknown. Here we show that Pescadillo/PES1, an estrogen-inducible protein that is over-expressed in breast cancer, can regulate the balance between ERM-NM-1 and ERM-NM-2. PES1 enhances transcriptional activity of ERM-NM-1 and reduces that of ERM-NM-2, and modulates many estrogen-responsive genes. Consistent with this regulation of ERM-NM-1 and ERM-NM-2 transcriptional activity, PES1 increases the stability of the ERM-NM-1 protein and decreases that of ERM-NM-2 through the ubiquitin-proteasome pathway, mediated by the carboxyl terminus of Hsc70-interacting protein (CHIP). Moreover, PES1 can transform normal human mammary epithelial cells and is required for estrogen-induced breast tumor growth in nude mice. Further analysis of clinical samples showed that expression of PES1 correlates positively with ERM-NM-1 expression and negatively with ERM-NM-2 expression, and predicts good clinical outcome in breast cancer. Our data demonstrate that PES1 contributes to breast tumor growth through regulating the balance between ERM-NM-1 and ERM-NM-2 and may be a better target for the development of drugs that selectively regulate ERM-NM-1 and ERM-NM-2 activities. Three samples: Control siRNA -E2 vs. Control siRNA +E2, Control siRNA -E2 vs. PES1 siRNA -E2,Control siRNA -E2 vs. PES1 siRNA +E2
2012-06-09 | E-GEOD-38621 | biostudies-arrayexpress
Project description:Estrogen receptor M-NM-1 (ERM-NM-1) is a nuclear receptor that is the driving transcription factor expressed in the majority of breast cancers. Recent studies have demonstrated that the liver receptor homolog-1 (LRH-1), another nuclear receptor, is ERM-NM-1-regulated in breast cancer cells. Further, LRH-1 stimulates proliferation and promotes motility and invasion of breast cancer cells. To determine the mechanisms of LRH-1 action in breast cancer cells, we carried out gene expression microarray analysis following siRNA-mediated LRH-1 knockdown. Interestingly, gene ontology (GO) category enrichment analysis of the genes differentially regulated in the presence or absence of LRH-1 identified estrogen responsive genes as the most highly enriched GO categories. To further define LRH-1 target genes, we performed chromatin immunoprecipitation coupled to massively parallel sequencing (ChIP-seq) to identify genomic targets of LRH-1. Remarkably, ChIP-seq showed LRH-1 binding at many ERM-NM-1 binding sites. Analysis of select binding sites confirmed regulation of ERM-NM-1-regulated genes by LRH-1 through binding to estrogen response elements, as exemplified by the TFF1/pS2 gene. Finally, LRH-1 over-expression stimulated ERM-NM-1 recruitment, whilst LRH-1 knockdown reduced ERM-NM-1 recruitment to ERM-NM-1 binding sites. Taken together, our findings establish a key role for LRH-1 in the regulation of ERM-NM-1 target genes in breast cancer cells and identify a mechanism in which co-operative binding of LRH-1 and ERM-NM-1 at estrogen response elements controls the expression of estrogen-responsive genes. MCF-7 cells were transfected with LRH-1 siRNA #2, #3, or with a non-targeting siRNA (siControl) for 72 hours. Following assessment of RNA integrity, four biological replicates for each siRNA treatment were used for microarray analysis.
2013-09-01 | E-GEOD-47803 | biostudies-arrayexpress
Project description:Investigation of whole genome gene expression level changes in SH-SY5Y cells transfected pCDNA3-Pea3, pCDNA3-Erm, and pCDNA3-Er81 cells compared to pCDNA3 transfected cells as a control.
2020-10-28 | E-MTAB-8473 | biostudies-arrayexpress
Project description:Investigation of whole genome gene expression level changes in mHypoA-2/12 cells transfected Pea3-pCDNA3, Erm-pCDNA3, and Er81-pCDNA3 cells compared to pCDNA3 transfected cells as a control.
2020-10-28 | E-MTAB-8475 | biostudies-arrayexpress
Project description:Study of differences in gene expression profiles in the mammary glands tumours of PEA3-null and wild-type PEA3 mice induced by the Her2/Neu transgene. Keywords: other
2005-12-09 | GSE3765 | GEO
Project description:COP1 regulates MAP kinase dependent stability Pea3 transcription factors. We determined the role of COP1 in the regulation of MAP kianse transciptional output. We transfected GIST882 cells with siRNA against a scrambled sequence and two sequences against COP1. We treated cells for 8 hours with vehicle or 100 nM PD0325901 in duplicate and isolated RNA for sequencing.
2018-04-15 | GSE80305 | GEO
Project description:Study of differences in gene expression profiles in the mammary glands tumours of PEA3-null and wild-type PEA3 mice induced by the Her2/Neu transgene. Experiment Overall Design: this experiment include 3 samples and 22 replicates
2008-06-12 | E-GEOD-3765 | biostudies-arrayexpress
Project description:The present experiments were performed to determine the roles of estrogen receptors M-NM-1 and M-NM-2 (ERM-NM-1 and ERM-NM-2) in normal and neoplastic development in the mouse mammary gland. In wild-type mice, in vivo administration of estradiol (E) + progesterone (P) stimulated mammary ductal growth and alveolar differentiation. Mammary glands from mice in which the ERM-NM-2 gene has been deleted (M-NM-2ERKO mice) demonstrated normal ductal growth and differentiation in response to E + P. By contrast, mammary glands from mice in which the ERM-NM-1 gene has been deleted (M-NM-1ERKO mice) demonstrated only rudimentary ductal structures that did not differentiate in response to E + P. EGF demonstrates estrogen-like activity in the mammary glands of M-NM-1ERKO mice: treatment of M-NM-1ERKO mice with EGF + P (without E) supported normal mammary gland development, induced expression of progesterone receptor (PR), and increased levels of G- protein-coupled receptor (GPR30) protein. Mammary gland development in M-NM-2ERKO mice treated with EGF + P was comparable to that of wild-type mice receiving EGF + P; EGF had no statistically significant effects on the induction of PR or expression of GPR30 in mammary glands harvested from either wild-type mice or M-NM-2ERKO mice. In vitro exposure of mammary glands to 7,12-dimethylbenz[a]anthracene (DMBA) induced preneoplastic mammary alveolar lesions (MAL) in glands from wild-type mice and M-NM-2ERKO mice, but failed to induce MAL in mammary glands from M-NM-1ERKO mice. Microarray analysis of DMBA-treated mammary glands identified 28 functional pathways whose expression was significantly different in M-NM-1ERKO mice versus both M-NM-2ERKO and wild-type mice; key functions that were differentially expressed in M-NM-1ERKO mice included cell division, cell proliferation, and apoptosis. The data demonstrate distinct roles for ERM-NM-1 and ERM-NM-2 in normal and neoplastic development in the mouse mammary gland, and suggest that EGF can mimic the ERM-NM-1-mediated effects of E in this organ. Gene expression of mammary gland organ culture and DMBA-induced lesions from 4 mouse strains.
2014-10-18 | E-GEOD-62451 | biostudies-arrayexpress