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Estrogen receptor beta repurposes EZH2 to suppress oncogenic NFκB signaling in triple negative breast cancer [ChIP-Seq]

ABSTRACT: Estrogen receptor beta repurposes EZH2 to suppress oncogenic NFκB signaling in triple negative breast cancer [ChIP-Seq]

PROVIDER: PRJNA655222 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12387600_1.fastq.gz	Fastqsanger.gz
	SRR12387600_2.fastq.gz	Fastqsanger.gz
	SRR12387601_1.fastq.gz	Fastqsanger.gz
	SRR12387601_2.fastq.gz	Fastqsanger.gz
	SRR12387602_1.fastq.gz	Fastqsanger.gz

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Estrogen receptor beta repurposes EZH2 to suppress oncogenic NFκB signaling in triple negative breast cancer

Project description:Estrogen receptor beta repurposes EZH2 to suppress oncogenic NFκB signaling in triple negative breast cancer

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Estrogen receptor beta repurposes EZH2 to suppress oncogenic NFκB signaling in triple negative breast cancer [RNA-Seq]

Project description:Estrogen receptor beta repurposes EZH2 to suppress oncogenic NFκB signaling in triple negative breast cancer [RNA-Seq]

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Estrogen receptor beta repurposes EZH2 to suppress oncogenic NFκB/p65 signaling in triple negative breast cancer.

Project description:Triple Negative Breast Cancer (TNBC) accounts for 15-20% of all breast cancer cases, yet is responsible for a disproportionately high percentage of breast cancer mortalities. Thus, there is an urgent need to identify novel biomarkers and therapeutic targets based on the molecular events driving TNBC pathobiology. Estrogen receptor beta (ERβ) is known to elicit anti-cancer effects in TNBC, however its mechanisms of action remain elusive. Here, we report the expression profiles of ERβ and its association with clinicopathological features and patient outcomes in the largest cohort of TNBC to date. In this cohort, ERβ was expressed in approximately 18% of TNBCs, and expression of ERβ was associated with favorable clinicopathological features, but correlated with different overall survival outcomes according to menopausal status. Mechanistically, ERβ formed a co-repressor complex involving enhancer of zeste homologue 2/polycomb repressive complex 2 (EZH2/PRC2) that functioned to suppress oncogenic NFκB/RELA (p65) activity. Importantly, p65 was shown to be required for formation of this complex and for ERβ-mediated suppression of TNBC. Our findings indicate that ERβ+ tumors exhibit different characteristics compared to ERβ- tumors and demonstrate that ERβ functions as a molecular switch for EZH2, repurposing it for tumor suppressive activities and repression of oncogenic p65 signaling.

| S-EPMC8854734 | biostudies-literature

Estrogen receptor beta repurposes EZH2 to suppress oncogenic NFκB signaling in triple negative breast cancer [ChIP-Seq]

Project description:The purpose of this study was to elucidate the effects of ERβ on the genomic distribution of NFκB and RNA Polymerase II phospho-Ser2, as well as changes in H3K27me3, H3K27ac, in MDA-MB-231 triple negative breast cancer cells.

2020-09-30 | GSE155684 | GEO

Estrogen receptor beta repurposes EZH2 to suppress oncogenic NFκB signaling in triple negative breast cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-09-30 | GSE155686 | GEO

Estrogen receptor beta repurposes EZH2 to suppress oncogenic NFκB signaling in triple negative breast cancer [RNA-Seq]

Project description:The purpose of this study was to elucidate the transcriptome of ERβ expressing MDA-MB-231 cells following treatment with veh, E2, TNFα, or E2+TNFα.

2020-09-30 | GSE155685 | GEO

Affinify Purification of EZH2 and phosphodeficient EZH2 identifies phosphorylation dependent interactions of EZH2

Project description:Overexpression of EZH2 in estrogen receptor negative (ER-) breast cancer promotes metastasis. EZH2 has been mainly studied as the catalytic component of the Polycomb Repressive Complex 2 (PRC2) that mediates gene repression by trimethylating histone H3 at lysine 27 (H3K27me3). However, how EZH2 drives metastasis despite the low H3K27me3 levels observed in ER- breast cancer is unknown. We have shown that in human invasive carcinomas and distant metastases, cytoplasmic EZH2 phosphorylated at T367 is significantly associated with ER- disease and low H3K27me3 levels. Here, we explore the interactome of EZH2 and of a phosphodeficient mutant EZH2_T367A. We identified novel interactors of EZH2, and identified interactions that are dependent on the phosphorylation and cellular localization of EZH2 that may play a role in EZH2 dependent metastatic progression.

2018-07-03 | PXD010073 | Pride

EZH2 is required for germinal center formation and somatic EZH2 mutations promote lymphoid transformation

Project description:The EZH2 histone methyltransferase is highly expressed in germinal center (GC) B-cells and targeted by somatic mutations in B-cell lymphomas. Here we find that EZH2 deletion or pharmacologic inhibition suppresses GC formation and functions in mice. EZH2 represses proliferation checkpoint genes and helps establish bivalent chromatin domains at key regulatory loci to transiently suppress GC B-cell differentiation. Somatic mutations reinforce these physiological effects through enhanced silencing of EZH2 targets in B-cells, and in human B-cell lymphomas. Conditional expression of mutant EZH2 in mice induces GC hyperplasia and accelerated lymphomagenesis in cooperation with BCL2. GCB-type DLBCLs are mostly addicted to EZH2, regardless of mutation status, but not the more differentiated ABC-type DLBCLs, thus clarifying the therapeutic scope of EZH2 targeting. RNA sequencing and H3K27me3 ChIP sequencing of human DLBCL cell lines and murine BCL1 cell line. RNA sequencing, H3K27me3 and H3K4me3 ChIP sequencing of B cells from de-identified human tonsills.

2013-05-13 | E-GEOD-45982 | biostudies-arrayexpress

Increased EZH2 function in regulatory T cells promotes their capacity to suppress autoimmunity by driving effector differentiation prior to activation [RNA-seq]

Project description:The immunosuppressive function of regulatory T (Treg) cells is essential for maintaining immune homeostasis. Enhancer of zeste homolog 2 (EZH2), a histone H3 lysine 27 (H3K27) methyltransferase, plays a key role in maintaining Treg cell function upon CD28 co-stimulation, and Ezh2 deletion in Treg cells causes autoimmunity. Here we assessed whether increased EZH2 activity in Treg cells would improve Treg cell function. Using an Ezh2 gain-of-function mutation, Ezh2Y641F, we found that Treg cells expressing Ezh2Y641F displayed an increased effector Treg phenotype and were poised for improved homing to organ tissues. Expression of Ezh2Y641F in Treg cells led to more rapid remission from autoimmunity. H3K27me3 profiling and transcriptomic analysis revealed a redistribution of H3K27me3, which prompted a gene expression profile in naïve Ezh2Y641F Treg cells that recapitulated aspects of CD28-activated Ezh2WT Treg cells. Altogether, increased EZH2 activity promotes the differentiation of effector Treg cells that can better suppress autoimmunity.

2024-09-10 | GSE262130 | GEO