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High content analysis of estrogen receptor activity: a mechanism-driven approach to compound testing

ABSTRACT: Analysis of the genome-wide response of the ER:PRL-HeLa cell line to treatment with estrogen receptor ligands estradiol, 4H-tamoxifen and bisphenol-A. Total RNA obtained from ER:PRL-HeLa cells treated for 4 hours with estradiol, 4H-tamoxifen or bisphenol -A is compared to vehicle treated controls

ORGANISM(S): Homo sapiens

SUBMITTER: David Loose

PROVIDER: E-GEOD-22941 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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High content analysis of estrogen receptor activity: a mechanism-driven approach to compound testing

Project description:Analysis of the genome-wide response of the ER:PRL-HeLa cell line to treatment with estrogen receptor ligands estradiol, 4H-tamoxifen and bisphenol-A.

2011-07-14 | GSE22941 | GEO

PRL-1 selectively dephosphorylates TIMELESS

Project description:The timing of behavior under natural light-dark conditions is a function of circadian clocks and photic input pathways. Yet a mechanistic understanding of how these pathways collaborate in animals is lacking. Here we demonstrate in Drosophila that the Phosphatase of Regenerating Liver-1 (PRL-1) sets period length and behavioral phase gated by photic signals. PRL-1 knockdown in PDF clock neurons dramatically lengthens circadian period. PRL-1 mutants exhibit allele-specific interactions with the light- and clock-regulated gene timeless (tim). Moreover, we show that PRL-1 promotes TIM accumulation and dephosphorylation. Interestingly, the PRL-1 mutant period lengthening is suppressed in constant light and PRL-1 mutants display a delayed phase under short, but not long, photoperiod conditions. Thus, our studies reveal that PRL-1 dependent dephosphorylation of TIM is a core mechanism of the clock that sets period length and phase in darkness, enabling the behavioral adjustment to changing day-night cycles.

2020-11-11 | PXD020986 | Pride

Gene expression profile in breast cancer cells

Project description:Human estrogen-responsive breast cancer cell line MCF-7 wt were used to produce stable clones expressing ER-beta tagged with TAP-tag respectively at the C-term and at the N-term (Ct-ER-beta and Nt-ER-beta) as previously described. MCF7 wt and beta clone cells were cultured in steroid-free medium for 5 days and then were treated with 10nM of 17-beta-estradiol, or vehicle (ETOH). RNA was extracted after 2h, 4h and 8h of stimulation with 17-ß-estradiol 10 nM (+E2) or ethanol vehicle . Total RNA extracted by Ct-ER-beta and Nt-ER-beta cells were pooled (TAP-ER-beta). For mRNA expression profiling, 500 ng total RNA were reverse transcribed and used for synthesis of cDNA and biotinylated cRNA. Finally cRNA were hybridized for 18 hours on Illumina HumanHT-12 v3.0 BeadChips and after scanning, data analysis was performed.

2011-07-29 | E-TABM-1051 | biostudies-arrayexpress

Expression profile of HEK293 cells stably transfected with PRL-1 (PTP4A1) or empty pcDNA4 vector (control)

Project description:The multifunctional protein tyrosine phosphatase PRL-1 (Gene Symbol: PTP4A1) has been identified as an important oncogene with roles in promoting cell proliferation, survival, migration, invasion, and metastasis. However, little is currently known about the signaling pathways through which it mediates its effects. We used Affymetrix Human Genome U133 Plus 2.0 arrays to examine the global molecular changes of gene expression occurring in response to stable PRL-1 overexpression in human embryonic kidney 293 (HEK293) cells. Total RNA was extracted from triplicate cultures of HEK293 cells stably overexpressing PRL-1 (HEK293-PRL-1) and HEK293 cells stably transfected with empty pcDNA4 vector (HEK293-Vector). Samples were hybridized to Affymetrix HG U133 Plus 2.0 microarrays (1 array per sample for a total of 6 arrays). One of the arrays hybridized with a PRL-1 transfected sample was excluded after qRT-PCR demonstrated that this sample did not exhibit increased PRL-1 expression over the level of the empty vector controls. The remaining 2 HEK293-PRL-1 samples both expressed PRL-1 at least 2-fold higher than any of the 3 empty vector controls.

2013-07-30 | E-GEOD-42586 | biostudies-arrayexpress

Quantitative real-time RT-PCR analysis of HEK293 cells stably transfected with PRL-1 (PTP4A1) or empty pcDNA4 vector control.

Project description:The protein tyrosine phosphatase PRL-1 (Gene Symbol: PTP4A1) has been identified as an important oncogene with roles in promoting cell proliferation, survival, migration, invasion, and metastasis. However, little is currently known about the signaling pathways through which it mediates its effects. Studies have shown a relationship between PRL-1 and the expression or activity levels of various molecules involved in integrin-mediated cell signaling. These integrin-responsive players can promote re-arrangements in the actin cytoskeleton that are central to cell motility, invasion, and metastasis. Therefore, to investigate the effects of PRL-1 overexpression in human embryonic kidney 293 (HEK293) cells, we used qRT-PCR to examine the expression levels of 184 genes which either were identified by microarray and proteomic analysis to be differentially expressed in response to PRL-1 or have known associations to integrin-mediated signaling, cytoskeletal remodeling, and/or cell motility. Total RNA was extracted from duplicate cultures of HEK293 cells stably overexpressing PRL-1 (HEK293-PRL-1) and HEK293 cells stably transfected with empty pcDNA4 vector (HEK293-Vector). Samples were analyzed using custom TaqMan Array 96-well Plates to examine the expression of 184 genes with known involvement in or association with signaling pathways related to integrin-mediated cell adhesion, cytoskeletal remodeling, and/or cell motility.

2013-07-30 | E-GEOD-42587 | biostudies-arrayexpress

Microarray analysis of multiple myeloma cell line INA-6 overexpressing PRL-3 vs. Mock control cells

Project description:PRL-3 is an oncogenic phosphatase, which is expressed at a higher level in malignant plasma cells from multiple myeloma patients than in plasma cells from healthy donors and high expression is associated with a poor prognosis. We overexpressed PRL-3 in a multiple myeloma cell line and our goal was to find signaling pathways regulated by PRL-3 in myeloma cells.

2021-07-01 | E-MTAB-10436 | biostudies-arrayexpress

Transcription profiling of human MCF-7 breast cancer cell line transfected with adenovirus expressing Erbeta treated with estrogen or tamoxifen reveals tamoxifen can selectively regulate a unique set of >60 genes, which are minimally regulated by estradiol (E2) or raloxifene.

Project description:The beneficial effect of the selective estrogen receptor (ER) modulator tamoxifen in the treatment and prevention of breast cancer is assumed to be through its ability to antagonize the stimulatory actions of estrogen, although tamoxifen can also have some estrogen-like agonist effects. Here, we report that, in addition to these mixed agonist/antagonist actions, tamoxifen can also selectively regulate a unique set of >60 genes, which are minimally regulated by estradiol (E2) or raloxifene in ERalpha-positive MCF-7 human breast cancer cells. This gene regulation by tamoxifen is mediated by ERalpha and reversed by E2 or ICI 182,780. Introduction of ERbeta into MCF-7 cells reverses tamoxifen action on approximately 75% of these genes. To examine whether these genes might serve as markers of tamoxifen sensitivity and/or the development of resistance, their expression level was examined in breast cancers of women who had received adjuvant therapy with tamoxifen. High expression of two of the tamoxifen-stimulated genes, YWHAZ/14-3-3z and LOC441453, was found to correlate significantly with disease recurrence following tamoxifen treatment in women with ER-positive cancers and hence seem to be markers of a poor prognosis. Our data indicate a new dimension in tamoxifen action, involving gene expression regulation that is tamoxifen preferential, and identify genes that might serve as markers of tumor responsiveness or resistance to tamoxifen therapy. This may have a potential effect on the choice of tamoxifen versus aromatase inhibitors as adjuvant endocrine therapy.

2007-10-02 | E-GEOD-4025 | biostudies-arrayexpress

Receptor-independent ectopic activity of PROLACTIN predicts aggressive lung tumors and indicates HDACi-based therapeutic strategies.

Project description:Aim: PROLACTIN (PRL), normally produced by the pituitary gland, acts through its receptor (PRL-R) to initiate a signalling cascade to the genome. PRL can also be produced by cancer cells and become oncogenic by stimulating its receptor following an autocrine or paracrine route. Here we investigated the oncogenic activities of PRL in lung cancer. Results: PRL is ectopically activated in a subset of very aggressive lung tumours, associated with a rapid fatal outcome, in our cohort of 293 lung tumour patients as well as in an external independent series of patients. An investigation of the molecular basis of PRL adverse effects surprisingly showed an absence of PRL-R expression in the vast majority of PRL-expressing lung tumours. Additionally, a detailed analysis of the ectopically expressed PRL transcripts in lung tumours and cell lines revealed systematic alterations of its first exons encoding the signal peptide. Finally, the transcriptomes of two PRL expressing lung cancer cell lines, with or without silencing of PRL, showed that PRL directly or indirectly sustains the expression of a group of genes that are frequently up-regulated in a variety of unrelated cancers. Interestingly, the gene signature repressed by PRL ectopic expression in lung tumour cells is also specifically up-regulated by HDAC inhibitor treatment or HDAC1/2/3 knock-down. Innovation and conclusion: Altogether, this work sheds lights on the poorly understood impact of the recently-shown large-scale out-of-context gene activity in cancer and also suggests that PRL-expressing aggressive lung cancers could be particularly responsive to a HDAC inhibitor-based treatment. Total RNA was extracted from two small cell lung carcinoma (SCLC) cell lines expressing PRL (H146 and h524: si control) or not (siPRL) and the differentially expressed genes. Five replicates were analysed for each of the four conditions.

2014-08-05 | E-GEOD-49544 | biostudies-arrayexpress

prolactin induced murine mammary carcinomas with different estrogen receptor status

Project description:8 independent mammary tumors (4 estrogen receptor alpha positive, 4 estrogen receptor negative by immunohistochemistry) that arose in nonparous NRL-PRL transgenic mice (FVB/N) were examined.

2011-01-15 | E-MEXP-3013 | biostudies-arrayexpress

MicroRNA profiling by array of human MCF-7 breast cancer cells with ER-beta tagged at the C-terminal or N-terminal and treated with 17-beta-estradiol

Project description:Human estrogen-responsive breast cancer cell line MCF-7 TET Off (MCF-7 wt) were used to produce stable clones expressing ER-beta tagged with TAP-tag respectively at the C-term and at the N-term (C-TAP-ER-beta and N-TAP-ER-beta) or expressing ER-alpha tagged (C-TAP-ER-alpha) as previously described.(C-TAP-ER-beta, N-TAP-ER-beta, C-TAP-ER-alpha) were treated with 10nM of17-beta-estradiol, or vehicle (ETOH). miRNA expression was analyzed on total RNA extracted before or after 6, 12, 24, and 72 hours hormonal stimulation. Total RNA was fluorescently labelled, amplified in triplicate, to be, than, pooled for the Hybridization.Each pool, were hybridized for 18 hours on Illumina v2 MicroRNA Expression BeadChips, and after scanning, analysis was performed with GenomeStudio v.2010.1 software, for quality control and miRNA expression analysis.

2011-07-29 | E-TABM-1055 | biostudies-arrayexpress

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