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U2OS-ERa, U2OS-ERb, and U2OS-ERab cells treated with 4HT or E2

ABSTRACT: U2OS-ERa, U2OS-ERb, and U2OS-ERab cells treated with 4HT or E2 Keywords: other

ORGANISM(S): Homo sapiens

PROVIDER: GSE2292 | GEO | 2005/04/06

SECONDARY ACCESSION(S): PRJNA91665

REPOSITORIES: GEO

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Transcription profiling of human U2OS cells expressing estrogen receptor alpha and beta heterodimers and treated with 17beta-estradiol or 4OH-tamoxifen

Project description:U2OS-ERa, U2OS-ERb, and U2OS-ERab cells treated with 4HT or E2

2007-08-25 | E-GEOD-2292 | biostudies-arrayexpress

Homo sapiens

Project description:U2OS-ERa, U2OS-ERb, and U2OS-ERab cells treated with 4HT or E2

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Estrogen effects on MCF-7 breast cancer cells co-expressing ERa and ERb

Project description:Two subtypes of the estrogen receptor, ERalpha and ERbeta, mediate the actions of estrogens, and the majority of human breast tumors contain both ERalpha and ERbeta. To examine the possible interactions and modulatory effects of ERbeta on ERalpha activity, we have used adenoviral gene delivery to produce human breast cancer (MCF-7) cells expressing ERbeta, along with their endogenous ERalpha. We have examined the effects of ERβ expression on genome-wide gene expression by Affymetrix GeneChip microarrays. We find that ERbeta modulated estrogen gene expression on nearly 24% of E2-stimulated genes but only 8% of E2-inhibited genes. We find that ERbeta modulation is gene-specific, enhancing or counteracting ERalpha regulation for distinct subsets of estrogen target genes. Introduction of ERbeta into ERalpha-containing cells induced up/down-regulation of many estrogen target in the absence of any added ligand. In addition, ERbeta presence elicited the expression of a unique set of genes that were not regulated by ERalpha alone. ERbeta modulated the expression of genes in many functional categories, but the greatest numbers were associated with transcription factor and signal transduction pathways. Regulation of multiple components in the TGF beta, SDF1, and semaphorin pathways, may contribute to the suppression of proliferation observed with ERbeta both in the presence and absence of estrogen. Hence, ERbeta modulates ERalpha gene regulation in diverse ways that may contribute to its growth-inhibiting beneficial effects in breast cancer Keywords: modulatory effects of ERb on ERa

2006-08-10 | GSE4006 | GEO

Transcription profiling of human colon cancer cell line SW480 expressing ERb and then treated with estrogen or untreated

Project description:Assess the full impact of estrogen receptor beta on transcription by a full transcriptome analysis of ERb-mediated gene regulation in the SW480 colon cancer cell line. The colon cancer cell line SW480 does not express endogenous ER but is made ERb-expressing by lentiviral transduction of an ERb expression cassette. Introduction of ERb makes it possible to study the role and function of ERb in colon cancer as well as the impact ERb has on its own (in the absence of ERa).

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Transcription profiling of breast cancer cells with TET-OFF regulated ERb expression treated with estradiol or ICI, an estrogen receptor antagonist

Project description:Assess the full impact of estrogen receptor beta on transcription by a full transcriptome analysis of ERa and ERb-mediated gene regulation in T47D breast cancer cell line with TET-OFF regulated ERb expression.

2007-12-17 | E-MEXP-969 | biostudies-arrayexpress

Assessment of transcriptional ERa activity following exposure to 17a-E2 and 17b-E2

Project description:Assessment of transcriptional ERa activity following exposure to 17a-E2 and 17b-E2

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RNA-seq data from MCF-7 cells (breast cancer model) treated with soy extracts

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Assessment of transcriptional ERa activity following exposure to 17a-E2 and 17b-E2

Project description:The study shows that, regardless of dose, both estrogens elicit nearly identical ERa activity

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RNA-seq data from MCF-7 cells (breast cancer model) treated with soy extracts

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2014-10-24 | E-GEOD-56066 | biostudies-arrayexpress

Ligand dependent gene regulation by transient ERa clustered enhancers

Project description:Unliganded Estrogen receptor alpha (ERa) has been implicated in ligand-dependent gene regulation. Upon ligand exposure, ERa binds to several EREs relatively proximal to the pre-marked, or persistent, ERa-bound sites and affects transient but robust gene expression. However, the underlying mechanisms are not fully understood. Here we demonstrate that upon ligand stimulation, persistent sites interact extensively, via chromatin looping, with the proximal transiently ERa-bound sites, forming Ligand Dependent ERa Enhancer Cluster in 3D (LDEC). The E2-target genes are regulated by these clustered enhancers but not by the H3K27Ac super-enhancers. Further, CRISPR-based deletion of TFF1 persistent site disrupts the formation of its LDEC resulting in the loss of E2-dependent expression of TFF1 and its neighboring genes within the same TAD. The LDEC overlap with nuclear ERa condensates that coalesce in a ligand and persistent site dependent manner. Furthermore, formation of clustered enhancers, as well as condensates, coincide with the active phase of signaling and their later disappearance results in the loss of gene expression even though persistent sites remain bound by ERa. Our results establish a direct link between ERa condensates, ERa enhancer clusters, and transient, but robust, gene expression in a ligand-dependent fashion.

2019-11-22 | GSE136302 | GEO

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