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Gene expression in response to progestin R5020

ABSTRACT: Breast cancer cell lines containing the progesterone receptor respond to progestins, altering expression of a subset of genes. In a previously published experiment of inducible knock-down of histone H1 isoforms with an shRNA-expression lentivector (GSE12299), we modified the breast cancer cell line T47D with different vectors. Here, we explored response to progestin R5020 of control cells generated with the empty shRNA-expression vector. Stable breast cancer-derived cell lines containing the empty vector for inducible shRNA expression were grown for two days in the absence of serum. Progestin R5020 or vehicle was added for 6 hours, in duplicate, and RNA was extracted for microarray hybridization.

ORGANISM(S): Homo sapiens

SUBMITTER: Lauro Sumoy

PROVIDER: E-GEOD-25077 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Progestins activate 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3) in breast cancer cells.

Novellasdemunt Laura L Obach Mercè M Millán-Ariño Lluís L Manzano Anna A Ventura Francesc F Rosa Jose Luis JL Jordan Albert A Navarro-Sabate Aurea A Bartrons Ramon R

The Biochemical journal 20120301 2

PFKFB (6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase) catalyses the synthesis and degradation of Fru-2,6-P2 (fructose-2,6-bisphosphate), a key modulator of glycolysis and gluconeogenesis. The PFKFB3 gene is extensively involved in cell proliferation owing to its key role in carbohydrate metabolism. In the present study we analyse its mechanism of regulation by progestins in breast cancer cells. We report that exposure of T47D cells to synthetic progestins (ORG2058 or norgestrel) leads to ...[more]

PMID: 22115192

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RNA-seq in two ER+ breast cancer cell lines with and without progestins

Project description:Exploring effect of progesterone/progestin treatment on gene expression Two cell lines, three conditions (Full Media with E2, E2+ Progesterone, Full Media + R5020 Progestin)

2015-05-22 | E-GEOD-68358 | biostudies-arrayexpress

Gene expression profiling of T47D breast cancer cells following progestin administration in presence or absence of Telapristone

Project description:Analysis of the effect of progesterone blockade at the gene expression level. The hypothesis tested in the present study is that elapristone (CDB4124), an antiprogestin, will downregulate genes that are stimulated by R5020, a synthetic progestin, in the T47D breast cancer cell line. Total RNA obtained from T47 breast cancer cells grown for 24 hours in the presence of: 1. The sythetic progestin R5020 compared to vehicle control; 2. The antiprogestin Telapristone (CDB4124) compared to vehicle control; and 3. R5020 compared to R5020 ± Telapristone.

2015-05-15 | E-GEOD-67561 | biostudies-arrayexpress

ChIP-seq of ER, PR, p300 in two ER+ breast cancer cell lines treated with estrogen and with and without progestins

Project description:Exploring effect of progesterone/progestin treatment on ER and PR binding. Two cell lines, three conditions (Full Media with E2, E2+ Progesterone, Full Media + R5020 Progestin), three factors (ER, PR, p300), all with three replicates, each with a matched Input control.

2015-05-22 | E-GEOD-68355 | biostudies-arrayexpress

Homo sapiens

Project description:Gene expression in response to progestin R5020

| PRJNA134745 | ENA

T47D_MTVL treatment with JAK/STAT inhibitor AG490 with/without R5020

Project description:Gene expression of the breast cancer cell line T47D-MTVL induced by progestin R5020, in the absense or presence of the JAK/STAT signaling pathway inhibitor AG490. Keywords: Gene expression - T47D-MTVL- hormonal treatment+inhibitors comparison

2007-10-12 | GSE9286 | GEO

PrPC-dependent gene expression and cell signalling signature in Neuro2a cells. Role on mitogenic stimulation and cell morphology.

Project description:In this work we present the PrPC-dependent gene expression signature in N2A cells and its implication on the most overrepresented functions; cell cycle, cell growth and proliferation and cell morphology. To evaluate the genes whose transcription was regulated after Prnp modulation, RNA samples were analyzed with Illumina mouse whole genome beadarrays. cell type comparison; genetic modification; RNA interference

2013-06-11 | E-GEOD-38887 | biostudies-arrayexpress

Prionic protein gene dosage is critical for maintenance of neuronal homeostasis of hippocampal circuits

Project description:We demonstrate that Prnp dosage is critical for the maintenance of neuronal homeostasis since both its absence and, more relevantly, its overexpression induce higher sensitivity to kainate (KA) damage. These data correlate with electrophysiological results in freely behaving mutant mice showing an imbalance in activity-dependent synaptic processes, as determined from input/output curves, paired-pulse facilitation, and LTP studies. Gene expression profiling showed that 129 genes involved in canonical pathways such as Ubiquitination or Neurotransmission among others were co-regulated in knockout and PrPc overexpressing mice. RT-qPCR analysis of neurotransmission-related genes confirmed GABA-A and AMPA-Kainate receptor subunit transcriptional co-regulation in both Prnp -/- and Tg20 mice. Our results demonstrate that PrPc is necessary for the proper homeostatic functioning of hippocampal circuits, because of its interactions with GABAA and AMPA-Kainate receptors. Keywords: steady state expression; adult brain tissue; hippocampus; genetic modification; transgenic gain of function mutation; targetted deletion loss of function mutation We performed a global transcriptome analysis of three strains that differ in their Prnp gene dose using Illumina Sentrix 6 mouse v1.1 beadarrays. We analyzed mRNA expression in the hippocampi of four individual male mice from each of three strains: 1) Tg20, with a 30 exogenous copies of the Prnp gene within a Prnp -/- background that overexpresses PrPc about 6-7 times the normal wild type levels; 2) littermates lacking the transgene and therefore carrying only the homozygous knock out Prnp -/- strain which lacks expression of PrPc; and 3) their wild type counterparts carrying two copies of the intact Prnp gene and expressing normal levels of PrPc

2010-04-09 | E-GEOD-16223 | biostudies-arrayexpress

Gene expression profiling of T47D breast cancer cells following progestin administration in presence or absence of Telapristone

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Nucleosome driven transcription factor binding and gene regulation [ChIP-Seq]

Project description:Elucidating the global function of a transcription factor implies the identification of its target genes and genomic binding sites. The role of chromatin in this context is unclear, but the dominant view is that factors bind preferentially to nucleosome-depleted regions, identified as DNaseI-hypersensitive sites (DHS). Here we show by chromatin-IP, MNase and DNaseI assays followed by deep sequencing that the progesterone receptor (PR) requires nucleosomes for optimal binding and function. In breast cancer cells treated with progestins we identified 25,000 PR binding sites (PRbs), the majority encompassing several copies of the hexanucleotide TGTYCY, highly abundant in the genome. We found that functional PRbs accumulate around progesterone-induced genes mainly in enhancers, are enriched in DHS but exhibit high nucleosome occupancy. Progestin stimulation results in remodeling of these nucleosomes with displacement of histones H1 and H2A/H2B dimers. Our results strongly suggest that nucleosomes are crucial for PR binding and hormonal gene regulation. T47D-MTVL human breast cancer cells were incubated with the progestin R5020 for different times between 0 to 360 minutes at 37ÂºC. ChIP-seq experiments were performed using antibodies against progesterone receptor and a single Sample each with anti-H3K4me3 and anti-H3K4me1. Mononucleosomal DNA was prepared from cells untreated or stimulated 60 min with R5020 and subjected to deep sequencing using the Solexa Genome Analyzer.

2012-12-01 | E-GEOD-41466 | biostudies-arrayexpress

Akt regulates Progesterone Receptor B transcription

Project description:Progestins have long been used clinically for the treatment of endometrial cancers, however, the response rates to progestin therapy vary and the molecular mechanisms behind progestin insensitivity are poorly understood. We hypothesized that in PTEN mutated endometrial cancers, hyperactive Akt signaling downregulates Progesterone Receptor B (PRB) transcriptional activity, leading to overall impaired progestin responses. We report that knockdown of Akt is sufficient to upregulate a subset of PRB target genes. PRB-Ishikawa endometrial cancer cells were transfected with either siCtrl or siAkt1, siAkt2, and siAkt3. Cells were then serum starved overnight and then treated with either Ethanol Vehicle Control or 10 nM R5020 for 24 hrs. Each treatment was performed in triplicate.

2015-09-04 | E-GEOD-72708 | biostudies-arrayexpress

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