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Gene expression profiles of MCF7 with with the following NR ligands: estradiol/E2 (ERα agonist), AM580 (RARA agonist), CD437 (RARG agonist), ATRA (RARA/RARG agonist), GW0742 (PPARD agonist), R5020 (PGR agonist), and dexamethasone (GR/NR3C1 agonist).

ABSTRACT: Altered gene expression patterns in human diseases reflect perturbations in the transcriptional networks that regulate cellular state. In breast cancer, Nuclear Receptors (NRs) play a prominent role in governing gene expression. NRs have prognostic utility and are therapeutically important targets. In order to understand the function of nuclear receptors in breast cancer, we treated MCF7 cells with 6 nuclear receptor agonist, and performed expression arrrays with three biological replicates each.

ORGANISM(S): Homo sapiens

PROVIDER: GSE42619 | GEO | 2013/01/01

SECONDARY ACCESSION(S): PRJNA182369

REPOSITORIES: GEO

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Gene expression profiles of MCF7 with with the following NR ligands: estradiol/E2 (ERÎ± agonist), AM580 (RARA agonist), CD437 (RARG agonist), ATRA (RARA/RARG agonist), GW0742 (PPARD agonist), R5020 (PGR agonist), and dexamethasone (GR/NR3C1 agonist).

Project description:Altered gene expression patterns in human diseases reflect perturbations in the transcriptional networks that regulate cellular state. In breast cancer, Nuclear Receptors (NRs) play a prominent role in governing gene expression. NRs have prognostic utility and are therapeutically important targets. In order to understand the function of nuclear receptors in breast cancer, we treated MCF7 cells with 6 nuclear receptor agonist, and performed expression arrrays with three biological replicates each. MCF-7 cells were cultured for 48 hours in medium with 10% charcoal-stripped FBS, and then were treated with 6 diffferent NR ligand (E2, AM580, CD437, ATRA, R5020, DEX) separately for 24h before collection and processing for microarrays. Three biological replicates were collected and processed for both control and treatment. with the 100nM GW0742 (PPARD specific ligand) and 100nM ATRA (RARs ligand), then collected after 24h for microarray processing. Controls were non-treated MCF7 cells. Both treatments and controls have three biological replicates.

2013-01-01 | E-GEOD-42619 | biostudies-arrayexpress

Gene expression profiles of MCF7 with with the following NR ligands: estradiol/E2 (ER? agonist), AM580 (RARA agonist), CD437 (RARG agonist), ATRA (RARA/RARG agonist), GW0742 (PPARD agonist), R5020 (PGR agonist), and dexamethasone (GR/NR3C1 agonist)

Project description: Not available

| S-ECPF-GEOD-42619 | biostudies-other

ChIP-chip of 38 nuclear receptors and NR co-factors in breast cancer cell line MCF7

Project description:Altered gene expression patterns in human diseases reflect perturbations in the transcriptional networks that regulate cellular state. In breast cancer, Nuclear Receptors (NRs) play a prominent role in governing gene expression. NRs have prognostic utility and are therapeutically important targets. Here we describe a complete regulatory map for twenty-four NR proteins that are expressed in the breast cancer cell line MCF-7, as well as fourteen additional breast cancer associated transcription factors (TFs) and six key chromatin state markers. The CEL files for the 38 NRs ChIP-chip presented in the paper are included, together with the results bar files, except 5 previsouly published ones: ER [GSE10800], RARA, RARG, FOXA1, GATA3 [GSE15244]. The supplementary bed file contains all 200,140 binding sites of all 38 TFs reported in the paper.

2013-01-01 | GSE41995 | GEO

DHT-AR, E2-AR and R5020-AR target gene profiles in LNCaP

Project description:We previously encountered regulatory processes where dihydrotestosterone (DHT) exerted its inhibitory effect on parathyroid hormone-related protein (PTHrP) gene repression through the estrogen receptor (ER)M-NM-1, but not the androgen receptor (AR) in breast cancer MCF-7 cells. Here, we investigated whether such an aberrant ligand-nuclear receptor (NR) interaction is present in prostate cancer LNCaP cells. First, we confirmed that LNCaP cells expressed a functional AR and at negligible levels of ERM-NM-1, and progesterone receptors. Both suppression of PTHrP and activation of the PSA genes were observed after treatment of E2, DHT and R5020. Consistent with the previous notion that the AR in LNCaP cells lost the ligand specificity due to a mutation AR (Thr-Ala877), our study using siRNA targeting each NR revealed that the AR, but not the other NRs, monopolized the role as the mediator of shared hormone-dependent regulation. These results were invariably associated with nuclear translocation of this mutant AR. Microarray of the genes regulated by either DHT, E2 or R5020 downstream of the AR (Thr-Ala877) revealed that more than half genes overlapped in LNCaP cells. Noticeably, AR (wild-type, wt) and AR (Thr-Ala877) were equally responsible for the E2-AR interactions. Fluorescent microscopic experiments demonstrated that both EGFP-AR (wt) and EGFP-AR (Thr-Ala877) were exclusively localized within the nucleus after E2 or DHT treatment. Further, a promoter assay revealed that breast cancer MCF-7 and Rv22 cells also exhibited such an aberrant E2-AR (wt) signaling. We postulate entangled interactions between the AR (wt) and E2 in a certain hormone-sensitive cancer cells. Total RNAs from the LNCaP cells transfected with control siRNA (siCT) or siRNA for AR (siAR) transfected LNCaP cells before 24 hr followed by exposed to 10-7M of DHT, E2 or R5020 exposure for another 24 h, respectively, were used.

2014-06-19 | E-GEOD-58615 | biostudies-arrayexpress

DHT-AR, E2-AR and R5020-AR target gene profiles in LNCaP

Project description:We previously encountered regulatory processes where dihydrotestosterone (DHT) exerted its inhibitory effect on parathyroid hormone-related protein (PTHrP) gene repression through the estrogen receptor (ER)α, but not the androgen receptor (AR) in breast cancer MCF-7 cells. Here, we investigated whether such an aberrant ligand-nuclear receptor (NR) interaction is present in prostate cancer LNCaP cells. First, we confirmed that LNCaP cells expressed a functional AR and at negligible levels of ERα, and progesterone receptors. Both suppression of PTHrP and activation of the PSA genes were observed after treatment of E2, DHT and R5020. Consistent with the previous notion that the AR in LNCaP cells lost the ligand specificity due to a mutation AR (Thr-Ala877), our study using siRNA targeting each NR revealed that the AR, but not the other NRs, monopolized the role as the mediator of shared hormone-dependent regulation. These results were invariably associated with nuclear translocation of this mutant AR. Microarray of the genes regulated by either DHT, E2 or R5020 downstream of the AR (Thr-Ala877) revealed that more than half genes overlapped in LNCaP cells. Noticeably, AR (wild-type, wt) and AR (Thr-Ala877) were equally responsible for the E2-AR interactions. Fluorescent microscopic experiments demonstrated that both EGFP-AR (wt) and EGFP-AR (Thr-Ala877) were exclusively localized within the nucleus after E2 or DHT treatment. Further, a promoter assay revealed that breast cancer MCF-7 and Rv22 cells also exhibited such an aberrant E2-AR (wt) signaling. We postulate entangled interactions between the AR (wt) and E2 in a certain hormone-sensitive cancer cells.

2014-06-19 | GSE58615 | GEO

Mechanism of inhibition of MMTV-neu and MMTV-wnt1 induced mammary oncogenesis by RARalpha agonist AM580.

Project description: Not available

| S-EPMC2891995 | biostudies-literature

Reversal by RARα agonist Am580 of c-Myc-induced imbalance in RARα/RARγ expression during MMTV-Myc tumorigenesis.

Project description: Not available

| S-EPMC3680916 | biostudies-literature

ChIP-chip of 6 chromatin marks (FAIRE, H3K4me1, H3K4me3, H3K27me3, H3R17me2, H3AZAce) in breast cancer cell line MCF7

2013-01-01 | E-GEOD-42617 | biostudies-arrayexpress

Effect of DC-SCRIPT expression in MCF7 breast cancer cell line

Project description:Breast cancer is one of the most common causes of cancer-related deaths in women. Nuclear receptors (NR) and their regulators are well known for their role in breast cancer. Especially ligands for the type I NRs, Estrogen Receptor (ER) and Progesterone Receptor have growth promoting effects in breast cancer cells. The NR coregulator DC-SCRIPT (ZNF366) has been found to be a strong and independent prognostic marker in ER positive (ESR1) breast cancer patients. DC-SCRIPT modulates the function of multiple NRs and has opposing effects on type I versus type II NRs. It represses the function of the growth promoting type I NRs, whereas it enhances the mainly anti-proliferative type II NRs. In this study we aimed to gain further insight into the functional role of DC-SCRIPT in breast cancer cells. Therefore, the effect of DC-SCRIPT expression on breast cancer cell gene expression was investigated using a novel DC-SCRIPT-inducible MCF7 breast cancer cell line model. In the presence of DC-SCRIPT, multiple cell cycle related genes were differentially expressed, including the tumor suppressor gene CDKN2B.

2015-08-01 | GSE59995 | GEO

ChIP-chip of 6 chromatin marks (FAIRE, H3K4me1, H3K4me3, H3K27me3, H3R17me2, H3AZAce) in breast cancer cell line MCF7

2013-01-01 | GSE42617 | GEO

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