Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

EZH2-mediated epigenetic suppression of IFNa/b-STAT2 signaling enhances anti-tumor immunity in breast cancer [RNA-Seq]

ABSTRACT: EZH2 knockdown or catylytic inhibition induces interferon signaling pathway

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE183458 | GEO | 2022/12/28

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

EZH2-mediated epigenetic suppression of IFNa/b-STAT2 signaling enhances anti-tumor immunity in breast cancer [ChIP-Seq]

Project description:Knockdown of catalytic inhibiton of EZH2 stimulates STAT2 recruitment in ISG promoter regions in luminal breast cancer cells

2022-12-28 | GSE183457 | GEO

EZH2-mediated epigenetic suppression of IFNa/b-STAT2 signaling enhances anti-tumor immunity in breast cancer

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

2022-12-28 | GSE183459 | GEO

EZH2-mediated epigenetic suppression of IFNa/b-STAT2 signaling enhances anti-tumor immunity in breast cancer

Project description:EZH2-mediated epigenetic suppression of IFNa/b-STAT2 signaling enhances anti-tumor immunity in breast cancer

| PRJNA760906 | ENA

EZH2-mediated epigenetic suppression of IFNa/b-STAT2 signaling enhances anti-tumor immunity in breast cancer [ChIP-Seq]

Project description:EZH2-mediated epigenetic suppression of IFNa/b-STAT2 signaling enhances anti-tumor immunity in breast cancer [ChIP-Seq]

| PRJNA760909 | ENA

EZH2-mediated epigenetic suppression of IFNa/b-STAT2 signaling enhances anti-tumor immunity in breast cancer [RNA-Seq]

Project description:EZH2-mediated epigenetic suppression of IFNa/b-STAT2 signaling enhances anti-tumor immunity in breast cancer [RNA-Seq]

| PRJNA760910 | ENA

Epigenetic regulation of cancer biology and anti-tumor immunity by EZH2.

Project description:Polycomb group proteins regulate chromatin structure and have an important regulatory role on gene expression in various cell types. Two polycomb group complexes (Polycomb repressive complex 1 (PRC1) and 2 (PRC2)) have been identified in mammalian cells. Both PRC1 and PRC2 compact chromatin, and also catalyze histone modifications. PRC1 mediates monoubiquitination of histone H2A, whereas PRC2 catalyzes methylation of histone H3 on lysine 27. These alterations of histones can lead to altered gene expression patterns by regulating chromatin structure. Numerous studies have highlighted the role of the PRC2 catalytic component enhancer of zeste homolog 2 (EZH2) in neoplastic development and progression, and EZH2 mutations have been identified in various malignancies. Through modulating the expression of critical genes, EZH2 is actively involved in fundamental cellular processes such as cell cycle progression, cell proliferation, differentiation and apoptosis. In addition to cancer cells, EZH2 also has a decisive role in the differentiation and function of T effector and T regulatory cells. In this review we summarize the recent progress regarding the role of EZH2 in human malignancies, highlight the molecular mechanisms by which EZH2 aberrations promote the pathogenesis of cancer, and discuss the anti-tumor effects of EZH2 targeting via activating direct anti-cancer mechanisms and anti-tumor immunity.

| S-EPMC5356764 | biostudies-literature

PRC2-Mediated Epigenetic Suppression of Type I IFN-STAT2 Signaling Impairs Antitumor Immunity in Luminal Breast Cancer.

Project description:The immunosuppressive tumor microenvironment in some cancer types, such as luminal breast cancer, supports tumor growth and limits therapeutic efficacy. Identifying approaches to induce an immunostimulatory environment could help improve cancer treatment. Here, we demonstrate that inhibition of cancer-intrinsic EZH2 promotes antitumor immunity in estrogen receptor α-positive (ERα+) breast cancer. EZH2 is a component of the polycomb-repressive complex 2 (PRC2) complex, which catalyzes trimethylation of histone H3 at lysine 27 (H3K27me3). A 53-gene PRC2 activity signature was closely associated with the immune responses of ERα+ breast cancer cells. The stimulatory effects of EZH2 inhibition on immune surveillance required specific activation of type I IFN signaling. Integrative analysis of PRC2-repressed genes and genome-wide H3K27me3 landscape revealed that type I IFN ligands are epigenetically silenced by H3K27me3. Notably, the transcription factor STAT2, but not STAT1, mediated the immunostimulatory functions of type I IFN signaling. Following EZH2 inhibition, STAT2 was recruited to the promoters of IFN-stimulated genes even in the absence of the cytokines, suggesting the formation of an autocrine IFN-STAT2 axis. In patients with luminal breast cancer, high levels of EZH2 and low levels of STAT2 were associated with the worst antitumor immune responses. Collectively, this work paves the way for the development of an effective therapeutic strategy that may reverse immunosuppression in cancer.SignificanceInhibition of EZH2 activates a type I IFN-STAT2 signaling axis and provides a therapeutic strategy to stimulate antitumor immunity and therapy responsiveness in immunologically cold luminal breast cancer.

| S-EPMC9772098 | biostudies-literature

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

Epigenetic antagonism between Snf5 and Ezh2 during oncogenic transformation

Project description:Epigenetic alterations have been increasingly implicated in oncogenesis. Analysis of Drosophila mutants suggests that Polycomb and SWI/SNF complexes can serve antagonistic developmental roles. However, the relevance of this relationship to human disease is unclear. Here we have investigated functional relationships between these epigenetic regulators in oncogenic transformation. Mechanistically, we show that loss of the SNF5 tumor suppressor leads to elevated expression of the Polycomb gene EZH2 and that Polycomb targets are broadly H3K27-trimethylated and repressed in SNF5-deficient fibroblasts and cancers. Further, we show antagonism between SNF5 and EZH2 in the regulation of stem cell-associated programs and that Snf5 loss activates those programs. Finally, using conditional mouse models, we show that inactivation of Ezh2 blocks tumor formation driven by Snf5 loss. Mouse Embryonic Fibroblasts (MEFs) conditionally inactivated for Ezh2, Snf5 and Ezh2, or from control WT MEFs were used to evaluated epigenetic antagonism between Snf5 and Ezh2 in the control of gene expression programs. Snf5-deficient lymphoma samples and control CD8+ WT T-cells were used to evaluate genetic programs misregulated by Snf5 inactivation during tumorigenesis. RNA was isolated from each of these samples and used for gene expression profiling on Affymetrix arrays.

2010-10-19 | E-GEOD-23656 | biostudies-arrayexpress

EZH2 Overexpression in Breast Cancer is due to MicroRNA-Dependent Suppression of ZBTB4

Project description:In order to Sp1 and EZH2-specific gene expression pattern in breast cancer, small interfering RNA for Sp1 and EZH2 was transfected in MDA-MB-231 cells. Four groups of samples are included: 1. si control (siCT_1, siCT_2, siCT_3). 2. siSp1 (siSp1_1, sisSp1_2, siSp1_3). 3. si control (siCT_A, siCT_B, siCT_C). 4. siEZH2 (siZEH2_1, siZEH2_2,siEZJ2_3). Gene expression profiles of Sp1 and EZH2 depleted cells were compared to that of siRNA controls. Experiments were performed in MDA-MB-231 cells.

2015-03-02 | E-GEOD-48979 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data