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USP10-mediated MOF (KAT8) stabilization accelerates the malignant progression of esophageal squamous cell carcinoma via epigenetically activating of ANXA2/Wnt signaling

ABSTRACT: USP10-mediated MOF (KAT8) stabilization accelerates the malignant progression of esophageal squamous cell carcinoma via epigenetically activating of ANXA2/Wnt signaling

PROVIDER: PRJNA1006336 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25663127_1.fastq.gz	Fastqsanger.gz
	SRR25663127_2.fastq.gz	Fastqsanger.gz
	SRR25663128_1.fastq.gz	Fastqsanger.gz
	SRR25663128_2.fastq.gz	Fastqsanger.gz
	SRR25663129_1.fastq.gz	Fastqsanger.gz

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USP10-mediated MOF (KAT8) stabilization accelerates the malignant progression of esophageal squamous cell carcinoma via epigenetically activating of ANXA2/Wnt signaling

Project description:Dysregulation of MOF (MYST1, KAT8), a highly conserved H4K16 acetyltransferase, plays important roles in human cancers. However, its expression and function in esophageal squamous cell carcinoma (ESCC) remain unknown. Here, we report that MOF is highly expressed in ESCC tumors and predicts a worse prognosis. Depletion of MOF in ESCC significantly impedes tumor growth and metastasis both in vitro and in vivo, whereas ectopic expression of MOF but not enzyme inactive mutant (MOF E350Q) promotes ESCC progression, suggesting that MOF acetyltransferase activity is crucial for its oncogenic activity. Further analysis reveals that USP10, a deubiquitinase highly expressed in ESCC, binds to and protects MOF from proteosome-dependent protein degradation. MOF stabilization by USP10 promotes H4K16ac enrichment in the ANXA2 promoter to stimulate ANXA2 transcription, which subsequently activates Wnt/ β-Catenin signaling to facilitate ESCC progression. Our findings highlight a novel USP10/MOF/ANXA2 axis as a promising therapeutic target for ESCC.

2024-01-09 | GSE241066 | GEO

Tudor-knot domain mutation in KAT8/MOF impede nucleosome interaction and histone acetylation [RNA-Seq]

Project description:KAT8 is a lysine acetyltransferase and is involved in multiple important biological processes including cancer. The well-known function of KAT8 is catalyzing acetylation on histone H4, which regulates gene expression and chromatin decompaction. Besides catalytic HAT domain, the function of Tudor-knot domain of KAT8 remains largely unclear. Here, we report a novel function of Tudor-knot domain in facilitates histone acetyltransferase activity on H4K16ac. One hot-spot cancer mutation on Tudor-knot domain of KAT8 inhibits its interaction with nucleosome and reduces H4K16ac level both in vitro and in cells without altering the chromatin occupancy. Interestingly, this Tudor-knot mutation does not influence acetylation activity of KAT8 on p53, a non-histone substrate, suggests the important function of KAT8 Tudor-knot domain in the substrate specific catalytic regulation.

2023-12-24 | GSE245008 | GEO

Tudor-knot domain mutation in KAT8/MOF impede nucleosome interaction and histone acetylation [ChIP-Seq]

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Tudor-knot domain mutation in KAT8/MOF impede nucleosome interaction and histone acetylation

Project description:Tudor-knot domain mutation in KAT8/MOF impede nucleosome interaction and histone acetylation

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RNA-sequencing data of THP-1 cells after the knockdown of KANSL2, KANSL3 or KAT8

Project description:Histone acetylation is associated with open chromatin and transcriptionally active genes. Specifically, acetylation of lysine 16 on histone H4 (H4K16ac) has been shown to prevent the assembly of nucleosomal arrays in vitro. This modification is catalyzed by the MYST-family histone acetyltransferase KAT8 (also known as MOF and MYST1), which is part of two distinct chromatin-associated complexes: NSL and MSL. While extensively studied in Drosophila, the functions of H4K16ac and the two KAT8-containing complexes in mammalian cells are not well understood. Here, we demonstrate a surprising complex-dependent activity of KAT8. We found that KAT8 catalyzes H4K5 and H4K8 acetylation as part of the NSL complex, whereas it catalyzes the bulk of H4K16 acetylation as part of the MSL complex. Furthermore, we show that the core proteins of the MSL complex and H4K16ac are not required for cell proliferation and global chromatin accessibility, whereas the NSL complex is essential for cell survival, as it is enriched at the promoters of housekeeping genes and is required for their transcription initiation. In summary, we show that KAT8 switches catalytic activity and function depending on its associated proteins, and that, as part of the NSL complex, it catalyzes H4K5 and H4K8 acetylation required for the expression of genes essential for cell survival.

2021-02-28 | GSE158521 | GEO

Tudor-knot domain mutation in KAT8/MOF impede nucleosome interaction and histone acetylation [RNA-Seq]

Project description:Tudor-knot domain mutation in KAT8/MOF impede nucleosome interaction and histone acetylation [RNA-Seq]

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Tudor-knot domain mutation in KAT8/MOF impede nucleosome interaction and histone acetylation [ChIP-Seq]

Project description:Tudor-knot domain mutation in KAT8/MOF impede nucleosome interaction and histone acetylation [ChIP-Seq]

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Complex-dependent histone acetyltransferase activity of KAT8 determines its role in transcriptional regulation and cellular homeostasis (ChIP-sequecing data)

2021-02-28 | GSE158736 | GEO

Next Generation Sequencing Analysis of Wild Type(WT) and Gdf9-Cre;Kat8 fl/fl(Kat8 Gdf9 cKO) Oocyte Transcriptome

Project description:Purpose: The goal of this study is to compare oocyte transcriptome profiling in WT and Kat8 Gdf9 cKO mice Methods: Oocyte mRNA profiles of 2 weeks old WT and Kat8 Gdf9 cKO mice were generated by deep sequencing using Illumina HiSeq 2500. Results: Using an optimized data analysis workflow, we mapped about 54-63 million sequence reads per sample to the mouse genome (build mm10) and identified 18,468 transcripts in the oocytes of WT and Kat8 Gdf9 cKO mice. Approximately 5% of the transcripts showed differential expression between the WT and Kat8 Gdf9 cKO oocyte, with a fold change ≥1.5 and p value <0.05. Conclusions: Our study represents the first detailed analysis of oocyte transcriptomes after kat8 deletion, which is generated by RNA-seq technology.Our results show that Kat8 affects numerous gene expression in mouse oocytes.

2017-03-25 | GSE97026 | GEO