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Activation of AKT induces EZH2-mediated β-catenin trimethylation in colorectal cancer. [Cut & Run]

ABSTRACT: Activation of AKT induces EZH2-mediated β-catenin trimethylation in colorectal cancer. [Cut & Run]

PROVIDER: PRJNA940747 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23698759.fastq.gz	Fastqsanger.gz
	SRR23698759_1.fastq.gz	Fastqsanger.gz
	SRR23698759_2.fastq.gz	Fastqsanger.gz
	SRR23698760.fastq.gz	Fastqsanger.gz
	SRR23698760_1.fastq.gz	Fastqsanger.gz

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Activation of AKT induces EZH2-mediated β-catenin trimethylation in colorectal cancer. [Cut & Run]

Project description:The lysine methyltransferase EZH2 is overexpressed in colorectal cancer (CRC) and has been found to be positively and negatively correlated with CRC patient survival depending on the study suggesting that EZH2 has a complex role in CRC. Here, we demonstrate that AKT-mediated EZH2 S21 phosphorylation induced EZH2 to trimethylate β-catenin at K49, which increased β-catenin’s binding to the chromatin. Additionally, EZH2-mediated β-catenin trimethylation induced β-catenin’s interaction with TCF1 and RNA polymerase II and resulted in a dramatic gain in genomic regions with β-catenin occupancy. Interestingly, EZH2 catalytic inhibition decreased stemness but increased migratory phenotypes of CRC cells with active AKT. Overall, we demonstrated that EZH2 modulates AKT-induced changes in gene expression through the AKT/EZH2/β-catenin axis in CRC. Our results suggest that EZH2 inhibitors have tumor-inhibiting and promoting effects in CRC as they inhibit EZH2-mediated methylation of histone and non-histone targets like β-catenin.

2023-08-23 | GSE226588 | GEO

Activation of AKT induces EZH2-mediated β-catenin trimethylation in colorectal cancer. [ChIP-Seq]

2023-08-23 | GSE226587 | GEO

Activation of AKT induces EZH2-mediated β-catenin trimethylation in colorectal cancer. [RNA-Seq]

2023-08-23 | GSE226584 | GEO

Activation of AKT induces EZH2-mediated β-catenin trimethylation in colorectal cancer.

Project description:Activation of AKT induces EZH2-mediated β-catenin trimethylation in colorectal cancer.

| PRJNA940741 | ENA

Activation of AKT induces EZH2-mediated β-catenin trimethylation in colorectal cancer. [ChIP-Seq]

Project description:Activation of AKT induces EZH2-mediated β-catenin trimethylation in colorectal cancer. [ChIP-Seq]

| PRJNA940740 | ENA

Activation of AKT induces EZH2-mediated β-catenin trimethylation in colorectal cancer. [RNA-Seq]

Project description:Activation of AKT induces EZH2-mediated β-catenin trimethylation in colorectal cancer. [RNA-Seq]

| PRJNA940739 | ENA

BRD9 functions as a methylarginine reader to regulate AKT-EZH2 signaling

Project description:Arginine methylation is a common posttranslational modification that is catalyzed by a family of protein arginine methyltransferases. Recognition of methylarginine marks by effector proteins (“readers”) is a critical link between arginine methylation and various cellular processes. We recently identified methylation of AKT1 at Arg391 by PRMT5, but the reader for this methylation has yet to be characterized. Here, we show that BRD9, a reader of acetylated lysine, unexpectedly recognizes Arg391-methylated AKT1 through an aromatic cage in its bromodomain. Disrupting the methylarginine reader function of BRD9 suppresses AKT activation and tumorigenesis. RNA-sequencing data shows that BRD9 and AKT co-regulate a hallmark transcriptional program in part through EZH2-mediated H3K27 trimethylation. Lastly, we find that inhibitors of BRD9 and EZH2 display synergistic effects on inhibition of cell viability and tumor growth. Together, our study demonstrates that BRD9 serves as a methylarginine reader to promote AKT-EZH2 oncogenic signaling and combined inhibition of BRD9 and EZH2 is a potential strategy for cancer therapy.

2025-03-18 | PXD058540 | Pride

CUT&RUN Sequencing of EZH2 binding sites in HEK293T cells expressing a Dual-specificity Aptamer that specifically increases O-GlcNAcylation on beta-catenin

Project description:O-GlcNAc is a dynamic post-translational modification on thousands of intracellular proteins, it regulates protein functions and is involved in many metabolic diseases. Using a dual-specificity aptamer, we targeted the O-GlcNAc transferase (OGT) to endogenous β-catenin and specifically increased O-GlcNAcylation of β-catenin. We found that O-GlcNAc on β-catenin promoted its interaction with EZH2 regardless of the Wnt signaling status. To study how this interaction regulates the distribution of EZH2 on the genome, we performed Cleavage Under Targets and Release Using Nuclease (CUT&RUN) on HEK293T cells expressing individual (Ctrl.) or dual-specificity aptamers. Under Wnt - and Wnt + conditions, the dual-specificity aptamer increased the binding of EZH2 on 923 and 3473 genomic sites, respectively. These two sets of differential binding sites showed little overlap.

2022-11-30 | GSE190172 | GEO

BRD9 functions as a methylarginine reader to regulate AKT-EZH2 signaling

2025-04-30 | GSE283326 | GEO

CUT&RUN Sequencing of EZH2 binding sites in HEK293T cells expressing a Dual-specificity Aptamer that specifically increases O-GlcNAcylation on beta-catenin, when beta-catein was knocked-down

Project description:O-GlcNAc is a dynamic post-translational modification on thousands of intracellular proteins, it regulates protein functions and is involved in many metabolic diseases. Using a dual-specificity aptamer, we targeted the O-GlcNAc transferase (OGT) to endogenous β-catenin and specifically increased O-GlcNAcylation of β-catenin. We found that O-GlcNAc on β-catenin promoted its interaction with EZH2 regardless of the Wnt signaling status. To study how this interaction regulates the distribution of EZH2 on the genome, we performed Cleavage Under Targets and Release Using Nuclease (CUT&RUN) on HEK293T cells expressing individual (Ctrl.) or dual-specificity aptamers, under Wnt - and Wnt + conditions. This is a control experiment in beta-catenin knockdown cells.

2022-10-11 | GSE214775 | GEO

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