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The SET Oncoprotein Promotes Estrogen-Induced Transcription by Facilitating Establishment of Active Chromatin

ABSTRACT: The SET Oncoprotein Promotes Estrogen-Induced Transcription by Facilitating Establishment of Active Chromatin

PROVIDER: PRJNA827161 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18776313.fastq.gz	Fastqsanger.gz
	SRR18776314.fastq.gz	Fastqsanger.gz
	SRR18776315.fastq.gz	Fastqsanger.gz
	SRR18776316.fastq.gz	Fastqsanger.gz
	SRR18776317.fastq.gz	Fastqsanger.gz

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The SET Oncoprotein Promotes Estrogen-Induced Transcription by Facilitating Establishment of Active Chromatin

Project description:The SET Oncoprotein Promotes Estrogen-Induced Transcription by Facilitating Establishment of Active Chromatin

| PRJNA905674 | ENA

The SET Oncoprotein Promotes Estrogen-Induced Transcription by Facilitating Establishment of Active Chromatin

Project description:SET is a multifunctional histone-binding oncoprotein that regulates transcription by an unclear mechanism. Here, we show that SET enhances estrogen-dependent transcription. SET knockdown abrogates transcription of estrogen-responsive genes and their enhancer RNAs (eRNAs). In response to 17β-estradiol (E2), SET binds to the estrogen receptor α (ERα) and is recruited to estrogen receptor α (ERα)-bound enhancers and promoters at estrogen response elements (EREs). SET functions as a histone H2 chaperone that dynamically associates with H2A.Z via its acidic C-terminal domain and promotes H2A.Z incorporation, ERα, MLL1 and KDM3A loading and modulates histone methylation at EREs. SET depletion diminishes recruitment of condensin complexes to EREs and impairs E2-dependent enhancer-promoter looping. Thus, SET boosts E2-induced gene expression by establishing an active chromatin structure at ERα-bound enhancers and promoters, which is essential for transcriptional activation.

2023-02-01 | GSE200900 | GEO

The SET Oncoprotein Promotes Estrogen-Induced Transcription by Facilitating Establishment of Active Chromatin

2023-02-02 | GSE218815 | GEO

The SET oncoprotein promotes estrogen-induced transcription by facilitating establishment of active chromatin.

Project description:SET is a multifunctional histone-binding oncoprotein that regulates transcription by an unclear mechanism. Here we show that SET enhances estrogen-dependent transcription. SET knockdown abrogates transcription of estrogen-responsive genes and their enhancer RNAs. In response to 17β-estradiol (E2), SET binds to the estrogen receptor α (ERα) and is recruited to ERα-bound enhancers and promoters at estrogen response elements (EREs). SET functions as a histone H2 chaperone that dynamically associates with H2A.Z via its acidic C-terminal domain and promotes H2A.Z incorporation, ERα, MLL1, and KDM3A loading and modulates histone methylation at EREs. SET depletion diminishes recruitment of condensin complexes to EREs and impairs E2-dependent enhancer-promoter looping. Thus, SET boosts E2-induced gene expression by establishing an active chromatin structure at ERα-bound enhancers and promoters, which is essential for transcriptional activation.

| S-EPMC9974495 | biostudies-literature

Combinatorial regulation of estrogen receptor alpha-responsive promoters

Project description:In breast cancer and normal estrogen target tissues, estrogen receptor alpha (ERalpha) signaling results in establishment of spatiotemporal patterns of gene expression. A time-course series of ChIP-chip experiments were performed to identify direct ERalpha target genes and determine whether these targets were transcriptionally activated or repressed by ERalpha. Keywords: Time-course ChIP-chip

2006-02-03 | GSE3987 | GEO

Coativator Function Defines the Active Estrogen Receptor Alpha Cistrome

Project description:Genome-wide ChIP-on-Chip against RNA Pol II in untreated MCF7 cells (phenol-red free media) and H3R17me2 in untreated and estrogen (45 min) treated cells.

2009-12-09 | GSE19328 | GEO

Differential gene expression between skin and cervix induced by the E7 oncoprotein in a transgenic mouse model

Project description:HPV16 E7 oncoprotein expression in K14E7 transgenic mice induces cervical cancer after 6 months of treatment with the co-carcinogen 17β-estradiol. In untreated mice, E7 also induces skin tumors late in life, albeit at low penetrance. These findings indicate that E7 alters cellular functions in cervix and skin so as to predispose these organs to tumorigenesis. Using microarrays, we determined the global genes expression profile in cervical and skin tissue of young adult K14E7 transgenic mice without estrogen treatment. In these tissues, the E7 oncoprotein altered the transcriptional pattern of genes involved in several biological processes, including immune response, intracellular signaling cascades, cell adhesion, cell migration, development, cell cycle, growth, response to wounding and regulation of apoptosis. Among the E7-dysregulated genes were ones not previously known to be involved in cervical neoplasia, including DMBT1, GLI1 and 17βHSD2 in cervix and MMP2, 12, 14, 19 and 27 in skin.

2012-06-10 | GSE36219 | GEO

Nuclear Estrogen Receptor alpha (ERα) interactome following estrogen and antiestrogen treatment.

Project description:The Estrogen Receptor alpha (ERα) controls key cellular functions in hormone responsive breast cancer by assembling in large functional multiprotein complexes. ERα ligands are classified as agonists and antagonist, according to the response they elicit, thus the molecular characterization of the of ERα nuclear iteractome composition following estrogen and antiestrogen stimulation whose is needed to understand their effects on estrogen target tissues, in particular breast cancer. To this aim interaction proteomics coupled to mass spectrometry (MS) was applied to map the ERα nuclear interacting partners in MCF7 breast cancer cell nuclei following estrogen and antiestrogen stimuli.

2020-09-02 | PXD018709 | Pride

Differential gene expression between skin and cervix induced by the E7 oncoprotein in a transgenic mouse model

Project description:HPV16 E7 oncoprotein expression in K14E7 transgenic mice induces cervical cancer after 6 months of treatment with the co-carcinogen 17M-NM-2-estradiol. In untreated mice, E7 also induces skin tumors late in life, albeit at low penetrance. These findings indicate that E7 alters cellular functions in cervix and skin so as to predispose these organs to tumorigenesis. Using microarrays, we determined the global genes expression profile in cervical and skin tissue of young adult K14E7 transgenic mice without estrogen treatment. In these tissues, the E7 oncoprotein altered the transcriptional pattern of genes involved in several biological processes, including immune response, intracellular signaling cascades, cell adhesion, cell migration, development, cell cycle, growth, response to wounding and regulation of apoptosis. Among the E7-dysregulated genes were ones not previously known to be involved in cervical neoplasia, including DMBT1, GLI1 and 17M-NM-2HSD2 in cervix and MMP2, 12, 14, 19 and 27 in skin. The experiment consists of a total of 24 samples to evaluate the mRNA expression profiles in 4 different groups: skin biopsy of transgenic mice K14E7, cervix biopsy of transgenic mice K14E7, skin biopsy of FVB/N control virgin mice and cervix biopsy of FVB/N control virgin mice. Each group has 6 samples that had been processed in 3 pools of two samples (biological replicates) for a total of 6 samples for each condition.

2012-06-09 | E-GEOD-36219 | biostudies-arrayexpress

SnoN oncoprotein enhances estrogen receptor-? transcriptional activity.

Project description:Estrogen receptor-? (ER?) and transforming growth factor-beta (TGF-?) signaling pathways are essential regulators during mammary gland development and tumorigenesis. Ski-related novel gene (SnoN) is an oncoprotein and a negative feedback inhibitor of TGF-? signaling. We have previously reported that low expression of SnoN in ER? positive breast carcinomas is associated with favorable prognosis (Zhang et al. Cancer Res. (2003) 63, 5005-5010). Here we have studied the mechanism of a possible cross-talk between ER? and SnoN. We find that SnoN interacts with the estrogen-activated form of ER? in the nucleus. SnoN contains two highly conserved nuclear receptor binding LxxLL-like motifs and we show that mutations in these motifs reduce the interaction of SnoN with ER?. Over-expression of SnoN enhanced the transcriptional activity of ER? in estrogen response element (ERE)-reporter assays, augmented the expression of several ER? target genes and increased the proliferation of MCF7 breast carcinoma cells in an estrogen-dependent manner. Chromatin immunoprecipitation demonstrated that SnoN interacts with ER? at the TTF1 (pS2) gene promoter. Conversely, silencing of SnoN reduced both ERE-reporter activity and the expression of ER? target genes in MCF7 and T-47D breast cancer cells. Histone deacetylase inhibition increased the level of SnoN and SnoN-dependent enhancement of ER?-dependent transcription and SnoN supported the recruitment of p300 histone acetylase to ER?. This study reveals a novel mechanism that interconnects ER? and TGF-? signaling pathways by SnoN. Accordingly, the results indicate that high SnoN level promotes ER? signaling and possibly breast cancer progression.

| S-EPMC3612938 | biostudies-literature

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