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RNA-seq in ARID1A WT, KO OVCA429 Cells after IFNγ treatment

ABSTRACT: RNA-seq in ARID1A WT, KO OVCA429 Cells after IFNγ treatment

PROVIDER: PRJNA545315 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9151850_1.fastq.gz	Fastqsanger.gz
	SRR9151850_2.fastq.gz	Fastqsanger.gz
	SRR9151860_1.fastq.gz	Fastqsanger.gz
	SRR9151860_2.fastq.gz	Fastqsanger.gz
	SRR9151851_1.fastq.gz	Fastqsanger.gz

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RNA-seq in ARID1A WT, KO OVCA429 Cells after IFNγ treatment

Project description:Whether cancer driver mutation(s) directly drives cancer immune phenotype and immune tolerance remains a standing question. ARID1A is a core member of the polymorphic BAF chromatin remodeling complex. ARID1A mutations frequently occur in human cancers and drive cancer development. Here, we studied the molecular, cellular, and clinical impact of ARID1A gene status on cancer immunity. We demonstrate that ARID1A mutations, limited expression, and deficiency impair interferon(IFN)-responsive gene chromatin accessibility and expression, resulting in anemic T cell tumor infiltration, weakened tumor immunity, and shortened host survival in many human cancer histologies as well as in murine cancer models, and are negatively associated with immunotherapy response. Mechanistically, ARID1A interacts with EZH2 via its carboxyl terminal and antagonizes EZH2-mediated IFN responsiveness. Thus, the interaction between ARID1A and EZH2 defines cancer IFN-responsiveness and immune evasion. Our work indicates that cancer epigenetic driver mutations can shape cancer immune phenotype and immunotherapy.

2020-05-06 | GSE131916 | GEO

RNA-seq transcriptonal profiling in partial hepatectomy liver tissues in Arid1a WT and liver specific KO mice.

Project description:Arid1a is the subunit of SWI/SNF complex, which was reported to guide SWI/SNF to DNA. Here, we found that loss of Arid1a in the liver results in improved liver regeneration after partial hepatectomy.Genome-wide analysis showed that after hepatectomy,loss of Arid1a reduces the recruitment and activity of E2F4 on target promoters, resulting in expression programs that favor regeneration during injury.RNAseq shows transcriptional profiling in WT and Arid1a LKO livers pre- and post-hepatectomy, which confirmed the E2F4 target genes and cell cycle genes were upregulated after hepatectomy. After partial hepatectomy, liver transcriptional profiling in WT and Arid1a liver specific KO mice were generated by RNA-seq analysis.

2016-03-30 | E-GEOD-76926 | biostudies-arrayexpress

ATAC-seq in ARID1A WT or KO OVCA429 Cells after interferron treatment

Project description:ATAC-seq in ARID1A WT or KO OVCA429 Cells after interferron treatment

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Intersection of ARID1A, EZH2 RNA-seq in OVCA429 cells with IFNγ treatment

Project description:Intersection of ARID1A, EZH2 RNA-seq in OVCA429 cells with IFNγ treatment

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Genome-wide gene expression analysis in treatment for 24 h with 40 μM APR-246 in ARID1A-WT and ARID1A-KO HCT116 cells.

Project description:To explore the sensitivity of ARID1A-KO cells to APR-246

2019-01-28 | GSE122925 | GEO

Loss of ARID1A leads to a cold tumor phenotype via suppression of IFNγ signaling

Project description:The collapse of inflammatory signaling that recruits cytotoxic immune cells to the tumor microenvironment contributes to the immunologically cold tumor phenotype in neuroblastoma (NB) and is a barrier to NB immunotherapy. Multiple studies have reported that MYCN amplification, a trait of high-risk NB, correlates with a loss of inflammatory signaling; but MYCN also correlates with 1p36 deletions in NB where the SWI/SNF chromatin remodeling complex subunit ARID1A (1p36.11) is located. ARID1A is known to support inflammatory signaling in adult cancers but its role in NB inflammatory signaling is unexplored. We find MYCN overexpression causes a stronger and ARID1A knockdown causes a weaker inflammatory response to interferon-gamma (IFNγ). ARID1A silencing reduces IFNγ induced gene signatures for the transcription factor interferon response factor 1 (IRF1). We found ARID1A is a functional interactor of IRF1 by co-immunoprecipitation studies, and ARID1A silencing causes loss of activating chromatin marks at the IRF1 target gene CXCL10. We model that IRF1 uses ARID1A containing SWI/SNF to promote IRF1’s target genes in response to IFNγ. This work finds that ARID1A is a critical regulator of inflammatory signaling in NB and provides rationale for testing immune therapies in MYCN amplified NB that are effective in adult ARID1A mutated cancers.

2025-01-01 | GSE277050 | GEO

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Project description:To investigate the function of Ptpn2, IFNγ and cGAS on axon regeneration, we performed gene transcription profiling of dorsal root ganglion neurons from 5 groups (WT, cKO, WT injured, cKO injured, RU521 injured) and retinal ganglion cells from 4 groups (WT, IFNγ, cKO, IFNγ+cKO).

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ATAC-seq in ARID1A WT or KO OVCA429 Cells after interferron treatment

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Genome-wide gene expression analysis in treatment for 24 h with 40 μM APR-246 in ARID1A-WT and ARID1A-KO HCT116 cells.

Project description:Genome-wide gene expression analysis in treatment for 24 h with 40 μM APR-246 in ARID1A-WT and ARID1A-KO HCT116 cells.

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DNA methylation statuses in ARID1A KO cells

Project description:The CpG island methylator phenotype (CIMP) is associated with prognosis and drug sensitivity in multiple cancer types. In gastric cancer, the CIMP is closely associated with Epstein-Barr virus (EBV) infection and AT-rich interactive domain 1A (ARID1A) mutations, a component of the SWI/SNF chromatin remodeling complex. However, the involvement of SWI/SNF defects in CIMP induction has been unclear. In this study, we demonstrate a causal role of ARID1A loss-of-function in CIMP induction. Mutations of SWI/SNF components, especially ARID1A, was associated with the CIMP, as well as EBV infection, in gastric cancers, and also in uterine endometrial and colorectal cancers, which are not affected by EBV infection. Genome-wide DNA methylation analysis showed that ARID1A knockout (KO) in cultured 293FT cells and gastric epithelial cells, GES1, induced aberrant DNA methylation of a substantial number of CpG sites. DNA methylation was induced at genomic regions with high levels of pre-existing histone H3 lysine 27 trimethylation (H3K27me3) and those with acquired H3K27me3 by ARID1A KO. These results showed that the ARID1A mutation induced aberrant DNA methylation, and this is likely to be one of the potential mechanisms of CIMP induction. (See GSE188293 for data of GES1 with ARID1A KO.)

2022-10-31 | GSE165239 | GEO

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