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EZH2 and JARID2 change their binding profiles on RNA and DNA to promote hepatocellular carcinoma [ChIP-seq]

ABSTRACT: EZH2 and JARID2 change their binding profiles on RNA and DNA to promote hepatocellular carcinoma [ChIP-seq]

PROVIDER: PRJNA553248 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9655620_1.fastq.gz	Fastqsanger.gz
	SRR9655620_2.fastq.gz	Fastqsanger.gz
	SRR9655630_1.fastq.gz	Fastqsanger.gz
	SRR9655630_2.fastq.gz	Fastqsanger.gz
	SRR9655621_1.fastq.gz	Fastqsanger.gz

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EZH2 and JARID2 change their binding profiles on RNA and DNA to promote hepatocellular carcinoma [ChIP-seq]

Project description:The molecular mechanisms of carcinogenesis have been deeply studied benefit from the highly developing biotechnologies. Here we used high throughput sequencing method to capture the global binding profiles on RNA and DNA of EZH2 and JARID2 in liver normal (THLE-2) and carcinoma (HepG2) cells, respectively. We found that EZH2 and JARID2 showed distinct binding profile in HepG2 and THLE-2 cells. By binding to the primary RNAs, bound transcripts of EZH2 and JARID2 in HepG2 showed significantly increased transcriptional level in hepatocellular carcinoma (HCC) patients. They bound transcripts were also highly related to the HCC development by performing gene set enrichment analysis (GSEA). By exploring the DNA binding profile, we also detected similar phenomena that EZH2 could increase the transcriptional level of bound genes in HepG2 cells, showing PRC2-independent functions in liver cancer cells. Integrating analysis of the RNA and DNA binding profile showed EZH2 could independent function at the transcriptional and post-transcriptional stages. In summary, we proposed that the novel regulatory functions of EZH2 and JARID2 that may promote the cancer development in carcinoma liver cells.

2022-07-04 | GSE133982 | GEO

EZH2 and JARID2 change their binding profiles on RNA and DNA to promote hepatocellular carcinoma [CLIP-seq]

2022-07-04 | GSE133980 | GEO

EZH2 and JARID2 change their binding profiles on RNA and DNA to promote hepatocellular carcinoma

Project description:EZH2 and JARID2 change their binding profiles on RNA and DNA to promote hepatocellular carcinoma

| PRJNA553245 | ENA

EZH2 and JARID2 change their binding profiles on RNA and DNA to promote hepatocellular carcinoma [CLIP-seq]

Project description:EZH2 and JARID2 change their binding profiles on RNA and DNA to promote hepatocellular carcinoma [CLIP-seq]

| PRJNA553247 | ENA

Functional Comparison to Ezh2 Reveals PRC2-Independent Functions of Jarid2 in Hematopoietic Stem Cell Lineage Commitment

Project description:Our previous studies showed the Polycomb Repressive Complex 2 (PRC2) co-factor Jarid2 represses self-renewal transcriptional networks in mouse multipotent progenitor cells (MPPs). But only a fraction of de-repressed HSC-specific genes were associated with loss of H3K27me3, implying Jarid2 may have non-canonical (PRC2-indpendent) in hematopoiesis. Here we sought to delineate any PRC2-independnent functions by comparing stem and progenitor cells genetically deficient for either Jarid2 or Ezh2. Loss of Ezh2 leads to increased myeloid differentiation in transplantation assays. In contrast, loss of Jarid2 enhanced T-cell output. Single cell transcriptomics showed while loss of Jarid2 had minimal impact across progenitor populations, loss of Ezh2 led to accumulation of lymphoid-biased MPP4 cells and B-cell progenitors in the bone marrow. Functional assays confirmed a differentiation block at the pre-pro B-cell stage. The maturational arrest of Ezh2-deficient B-cell progenitors contrasts with increased T-cell output from loss of Jarid2, suggesting Jarid2 has non-canonical functions in hematopoiesis.

2025-11-17 | GSE302605 | GEO

Jarid2 and PRC2, Partner in Regulating Gene Expression

Project description:The Polycomb Group proteins foster gene repression profiles required for proper development and unimpaired adulthood, and comprise the components of the PRC2 complex including the histone H3 lysine 27 (H3K27) methyltransferase Ezh2. How mammalian PRC2 accesses chromatin is unclear. We find that Jarid2 associates with PRC2 and stimulates its enzymatic activity in vitro. Jarid2 contains a Jumonji C domain, but is devoid of detectable histone demethylase activity. Instead, its artificial recruitment to a promoter in vivo resulted in co-recruitment of PRC2 with resultant increased levels of H3K27me2/3. Jarid2 co-localizes with Ezh2 and MTF2, a homologue of Drosophila Pcl, at endogenous genes in ES cells. Jarid2 can itself bind DNA and its recruitment in ES cells is interdependent with that of PRC2 as Jarid2 knockdown reduced PRC2 at its target promoters, and ES cells devoid of the PRC2 component EED are deficient in Jarid2 promoter access. In addition to the well-documented defects in embryonic viability upon down-regulation of Jarid2, ES cell differentiation is impaired, as is Oct4 silencing. Examination of two factors in ES cells

2010-01-01 | E-GEOD-19708 | biostudies-arrayexpress

Jarid2 and PRC2, Partner in Regulating Gene Expression

2010-01-01 | GSE19708 | GEO

Jarid2/Jumonji coordinates control of PRC2 enzymatic activity and target gene occupancy in pluripotent cells

Project description:We report on mechanism of interaction between PRC2 complex and Jarid2 and their role in pluripotent cells Examination of PRC2 genomic localization by analysis of Jarid2, Ezh2, Suz12 and Jarid1a occupancy

2009-12-24 | E-GEOD-18776 | biostudies-arrayexpress

EZH2 and JARID2 change their binding profiles on RNA and DNA to promote hepatocellular carcinoma

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

2022-07-04 | GSE133984 | GEO

EZH2 deficiency induced gene expression change in CRCs

Project description:EZH2 deficiency induced gene expression change in CRCs

| PRJNA668530 | ENA