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EZH2 T367 phosphorylation activates p38 signaling through lysine methylation to promote breast cancer progression [RNA-seq]

ABSTRACT: EZH2 T367 phosphorylation activates p38 signaling through lysine methylation to promote breast cancer progression [RNA-seq]

PROVIDER: PRJNA857078 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20063583.fastq.gz	Fastqsanger.gz
	SRR20063584.fastq.gz	Fastqsanger.gz
	SRR20063585.fastq.gz	Fastqsanger.gz
	SRR20063586.fastq.gz	Fastqsanger.gz
	SRR20063587.fastq.gz	Fastqsanger.gz

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EZH2 T367 phosphorylation activates p38 signaling through lysine methylation to promote breast cancer progression

Project description:EZH2 T367 phosphorylation activates p38 signaling through lysine methylation to promote breast cancer progression

| PRJNA857076 | ENA

EZH2 T367 phosphorylation activates p38 signaling through lysine methylation to promote breast cancer progression [ChIP-seq]

Project description:EZH2 T367 phosphorylation activates p38 signaling through lysine methylation to promote breast cancer progression [ChIP-seq]

| PRJNA857079 | ENA

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 T367 phosphorylation activates p38 signaling through lysine methylation to promote breast cancer progression.

Project description:Triple-negative breast cancers (TNBCs) are frequently poorly differentiated with high propensity for metastasis. Enhancer of zeste homolog 2 (EZH2) is the lysine methyltransferase of polycomb repressive complex 2 that mediates transcriptional repression in normal cells and in cancer through H3K27me3. However, H3K27me3-independent non-canonical functions of EZH2 are incompletely understood. We reported that EZH2 phosphorylation at T367 by p38α induces TNBC metastasis in an H3K27me3-independent manner. Here, we show that cytosolic EZH2 methylates p38α at lysine 139 and 165 leading to enhanced p38α stability and that p38 methylation and activation require T367 phosphorylation of EZH2. Dual inhibition of EZH2 methyltransferase and p38 kinase activities downregulates pEZH2-T367, H3K27me3, and p-p38 pathways in vivo and reduces TNBC growth and metastasis. These data uncover a cooperation between EZH2 canonical and non-canonical mechanisms and suggest that inhibition of these pathways may be a potential therapeutic strategy.

| S-EPMC9389258 | biostudies-literature

EZH2 T367 phosphorylation activates p38 signaling through lysine methylation to promote breast cancer progression

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

2022-07-12 | GSE207796 | GEO

Effect of T350 phosphorylation on gene repression activity of EZH2 in BJ cells

Project description:The Polycomb group (PcG) protein enhancer of zeste homolog 2 (EZH2) plays an essential role in histone methylation-mediated epigenetic gene silencing. We demonstrate that under physiological conditions, cyclin-dependent kinase 1 (CDK1) and 2 (CDK2) bind to and phosphorylate EZH2 at threonine 350 (T350) in an evolutionally conserved motif. T350 phosphorylation is required for EZH2 function in silencing of genes that promote differentiation and inhibit proliferation and migration. Blockage of T350 phosphorylation by generating a T350A mutation largely diminishes the global effect of EZH2 on gene silencing. Four experiments have been designed. BJ cells were transfected with si-Control, si-EZH2, si-EZH2 plus RNAi resistant lentivirus expressed EZH2, or si-EZH2 plus RNAi resistant lentivirus expressed T350A mutant for 60 hours. Each experiment was triplicated.

2010-11-10 | E-GEOD-22427 | biostudies-arrayexpress

p38 MAPK-dependent phosphorylation of TFEB promotes monocyte-to-macrophage differentiation

Project description:The transcription factor EB (TFEB) regulates energy homeostasis and cellular response to a wide variety of stress conditions, including nutrient deprivation, oxidative stress, organelle damage, and pathogens. Here we identify S401 as a novel phosphorylation site within the TFEB proline-rich domain. Phosphorylation of S401 increases significantly in response to oxidative stress, UVC light, growth factors and LPS, whereas this increase is prevented by p38 MAPK inhibition or depletion, revealing a new role for p38 MAPK in TFEB regulation. Mutation of S401 in THP1 cells demonstrates that the p38 MAPK/TFEB pathway plays a particularly relevant role during monocyte differentiation into macrophages. TFEB-S401A monocytes fail to upregulate expression of multiple immune genes in response to PMA-induced differentiation, including critical cytokines, chemokines, and growth factors. Polarization of M0 macrophages into M1 inflammatory macrophages is also aberrant in TFEB-S401A cells. These results indicate that TFEB-S401 phosphorylation links differentiation signals to the transcriptional control of monocyte differentiation.

2022-12-06 | GSE217608 | GEO

EZH2 T367 phosphorylation activates p38 signaling through lysine methylation to promote breast cancer progression [RNA-seq]

Project description:To investigate the gene expression deregulation in Breast Cancer Tumors treated with P38i, EZH2i, the combination and controls.

2022-07-12 | GSE207795 | GEO

EZH2 T367 phosphorylation activates p38 signaling through lysine methylation to promote breast cancer progression [ChIP-seq]

Project description:To investigate the differential abundance of H3k27me3 mark on the promoters of Breast Cancer cells treated with P38i, EPZi, the combination and controls

2022-07-12 | GSE207794 | GEO

p38 MAPK-dependent phosphorylation of TFEB promotes monocyte-to-macrophage differentiation

Project description:In addition to the role in lysosomal biogenesis and autophagy, TFEB has been described to participate in the control of inflammation and host defense against pathogen infection The activation of TFEB in toll-like receptor-induced or bacteria exposed macrophages is regulated by a mechanism independent of mTORC1 inactivation, suggesting that other protein kinases may participate in the regulation of TFEB function during macrophage activation In this study, we identified a novel role of p38 MAPK in TFEB regulation. We showed p38-dependent TFEB phosphorylation at serine 401 (S401) in response to a variety of stress conditions, including oxidative stress, UVC irradiation, growth factors, and lipopolysaccharide (LPS) treatment. Furthermore, inhibition of S401 phosphorylation during PMA-induced monocyte differentiation prevented TFEB nuclear accumulation and resulted in reduced expression of multiple immune genes. TFEB-S401A expressing M0 macrophages also failed to efficiently polarize into M1 inflammatory macrophages, showing defective upregulation of cytokines and chemokines, as well as reduced inflammasome activation. We conclude that TFEB is a target of the p38 signaling pathway that is required for monocyte/macrophage differentiation and function.

2022-12-06 | GSE201826 | GEO

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