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Mus musculus

ABSTRACT: Time course of myeloid differentiation in the Lysozyme-GFP ER-HoxA9 cells following estradiol withdrawal

OTHER RELATED OMICS DATASETS IN: GSE84875

PROVIDER: PRJNA335412 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3954160_1.fastq.gz	Fastqsanger.gz
	SRR3954160_2.fastq.gz	Fastqsanger.gz
	SRR3954170_1.fastq.gz	Fastqsanger.gz
	SRR3954170_2.fastq.gz	Fastqsanger.gz
	SRR3954180_1.fastq.gz	Fastqsanger.gz

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Time course of myeloid differentiation in the Lysozyme-GFP ER-HoxA9 cells following estradiol withdrawal

Project description:Lysozyme-GFP ER-HoxA9 cells were cultured in the presence of estradiol (active ER-HoxA9) or in the absence of estradiol (inactive ER-HoxA9). Samples were taken at 10 time points over a 120 hour time course of myeloid differentiation to examine those gene expression changes that accompany differentiation upon the release of HoxA9 differentiation arrest.

2016-10-01 | GSE84874 | GEO

Gene expression changes after loss of Hoxa9 in transformed HSCs [HOXA9 RNA-seq]

Project description:Characterization of gene expression changes 72 hours after withdrawal of tamoxifen in murine hematopoietic progenitors transformed by Hoxa9-ER/Meis1 using RNAseq. In the presence of tamoxifen (4OHT), Hoxa9-ER localizes to the nucleus of cells allowing for transformation, while withdrawal of 4OHT (culture in EtOH) leads to loss of nuclear Hoxa9-ER. Loss of Hoxa9-ER leads to a decrease in cellular proliferation and differentiation along the myeloid lineage.

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Gene expression changes after loss of Hoxa9 in transformed HSCs [HOXA9 RNA-seq]

2014-06-11 | E-GEOD-58359 | biostudies-arrayexpress

RNAseq of murine primary bone marrow cells transformed by an inducible Hoxa9-ER: time-course

Project description:Relative overexpression of HOXA9 is a key feature of aggressive AML (acute myeloid leukemia). Hoxa9 responsive genes were identified by nascent RNA sequencing (4-thio-uridine labeled RNA - sequencing) in samples of primary hematopoietic precursor cells from mice transformed by an tamoxifen inducible version of Hoxa9 (Hoxa9-ER). Samples were generated in the presence of active Hoxa9 (0h) and in a time series after Hoxa9 was inactivated at 8h, 16h, 24h, 48h, and 72h.

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ATAC-seq profiling of ER-Hoxa9-Lys-GFP cells over myeloid differentiation program

Project description:ATAC-seq profiling of ER-Hoxa9-Lys-GFP cells over myeloid differentiation program

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Transcription profiling of mouse erythroleukemia cells following activation of Gata1-ER or PU.1-ER transgenes

Project description:17b-Estradiol added to MEL cells expressing Gata1-ER or PU.1-ER transgenes to stimulate either erythropoietic Gata-1 dependent or myeloid PU.1 dependent gene espression in different time points

2009-09-30 | E-MTAB-125 | biostudies-arrayexpress

Identification of genome wide Hoxa9 binding sites in primary murine and human AML cells

Project description:Relative overexpression of HOXA9 is a key feature of aggressive AML (acute myeloid leukemia). Here we determined genome wide binding sites of Hoxa9 in primary murine cells transformed by Hoxa9 and in a human AML cell line. In addition global H3K4 monomethylation and H3K27acetylation levels were determined in cells transformed by an inducible Hoxa9-ER construct in Hoxa9-active conditions and 72h after Hoxa9 was inactivated.

2019-04-13 | E-MTAB-7108 | biostudies-arrayexpress

Time-course effect of estradiol and estradiol-BSA on early gene expression

Project description:This SuperSeries is composed of the following subset Series: GSE32666: Time-course effect of estradiol and estradiol-BSA on early gene expression in T47D cells GSE32667: Time-course effect of estradiol and estradiol-BSA on early gene expression in MCF-7 cells GSE32668: Time-course effect of estradiol and estradiol-BSA on early gene expression in MDA-MB-231 cells GSE32669: Time-course effect of estradiol and estradiol-BSA on early gene expression in SKBR3 cells Refer to individual Series

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Profiling of ER+ BrC cells with and without estradiol in both cell cultures and xenografts

Project description:We generated DNA microarray based gene expression profiles from three estrogen receptor a (ERa) positive breast cancer cell lines stimulated by 17ß-estradiol (E2) in vitro over a time course, as well as from MCF-7 cells grown as xenografts in ovariectomized athymic nude mice with E2 supplementation and after its withdrawal. Keywords: Cell line and xenograft comparisons

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Genome-wide copy number profiling of MCF-7 and fulvestrant-resistant MCF-7/FR cells by SNP microarray.

Project description:Estrogens have been shown to elicit anti-cancer effects against estrogen receptor alpha (ER)-positive breast cancer. We sought to determine the underlying mechanism of therapeutic response. Response to 17b-estradiol was assessed in ER+ breast cancer models with resistance to estrogen deprivation: WHIM16 patient-derived xenografts, C7-2-HI and C4-HI murine mammary adenocarcinomas, and long-term estrogen-deprived MCF-7 cells. As another means to reactivate ER, the anti-estrogen fulvestrant was withdrawn from fulvestrant-resistant MCF-7 cells. Transcriptional, growth, apoptosis, and molecular alterations in response to ER reactivation were measured. 17b-estradiol treatment and fulvestrant withdrawal induced transcriptional activation of ER, and cells adapted to estrogen deprivation or fulvestrant were hypersensitive to 17b-estradiol. ER transcriptional response was followed by an unfolded protein response and apoptosis. Such apoptosis was dependent upon the unfolded protein response, p53, and JNK signaling. Anti-cancer effects were most evident in models exhibiting genomic amplification of the gene encoding ER (ESR1), suggesting that engagement of ER at high levels is cytotoxic. These data indicate that long-term adaptation to estrogen deprivation or ER inhibition alters sensitivity to ER reactivation. In such adapted cells, 17b-estradiol treatment and anti-estrogen withdrawal hyperactivate ER, which drives an unfolded protein response activation and subsequent growth inhibition and apoptosis. 17b-estradiol treatment should be considered as an alternative therapy for anti-estrogen-resistant disease, particularly in patients with tumors harboring ESR1 amplification or overexpression. Furthermore, therapeutic strategies that enhance an unfolded protein response may enhance the therapeutic effects of ER reactivation.

2019-08-19 | GSE121631 | GEO

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