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ARID1A deficiency weakens BRG1-RAD21 interaction that jeopardizes chromatin compactness and drives HCC metastasis [ChIP-seq]

ABSTRACT: ARID1A deficiency weakens BRG1-RAD21 interaction that jeopardizes chromatin compactness and drives HCC metastasis [ChIP-seq]

PROVIDER: PRJNA638150 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11955380_1.fastq.gz	Fastqsanger.gz
	SRR11955380_2.fastq.gz	Fastqsanger.gz
	SRR11955381_1.fastq.gz	Fastqsanger.gz
	SRR11955381_2.fastq.gz	Fastqsanger.gz
	SRR11955382_1.fastq.gz	Fastqsanger.gz

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ARID1A deficiency weakens BRG1-RAD21 interaction that jeopardizes chromatin compactness and drives HCC metastasis

Project description:ARID1A deficiency weakens BRG1-RAD21 interaction that jeopardizes chromatin compactness and drives HCC metastasis

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ARID1A deficiency weakens BRG1-RAD21 interaction that jeopardizes chromatin compactness and drives HCC metastasis [RNA-seq]

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ARID1A deficiency weakens BRG1-RAD21 interaction that jeopardizes chromatin compactness and drives HCC metastasis [ChIP-seq]

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ARID1A deficiency weakens BRG1-RAD21 interaction that jeopardizes chromatin compactness and drives HCC metastasis [RNA-seq]

Project description:ARID1A deficiency weakens BRG1-RAD21 interaction that jeopardizes chromatin compactness and drives HCC metastasis [RNA-seq]

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ARID1A deficiency weakens BRG1-RAD21 interaction that jeopardizes chromatin compactness and drives liver cancer cell metastasis.

Project description:ARID1A, encoding a subunit of SWI/SNF chromatin remodeling complex, is widely recognized as a tumor suppressor gene in multiple tumor types including liver cancer. Previous studies have demonstrated that ARID1A deficiency can cause liver cancer metastasis, possibly due to the altered chromatin organization, however the underlying mechanisms remain poorly understood. To address the effect of Arid1a deficiency on chromatin organization, we generated chromatin interaction matrices, and exploited the conformation changes upon Arid1a depletion in hepatocytes. Our results demonstrated that Arid1a deficiency induced A/B compartment switching, topologically associated domain (TAD) remodeling, and decrease of chromatin loops. Further mechanism studies revealed that ATPase BRG1 of SWI/SNF complex could physically interact with RAD21, a structural subunit of chromatin architectural element cohesin; whereas ARID1A deficiency significantly diminished the coupled BRG1-RAD21. Interestingly, the tumor-associated genes within the switched compartments were differentially expressed depending upon Arid1a depletion or not. As a consequence of ARID1A deficiency-induced conformational alteration, the dysregulation of some genes such as PMP22 and GSC, promoted the invasion capacity of liver cancer cells. This study provides an insight into liver cancer tumorigenesis and progression related to ARID1A mutations.

| S-EPMC8542038 | biostudies-literature

ARID1A deficiency weakens BRG1-RAD21 interaction that jeopardizes chromatin compactness and drives HCC metastasis

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

2020-08-24 | GSE152052 | GEO

Expression analysis of Vitis Vinifera clones differing for compactness

Project description:Grapevine cluster compactness is a multi-componential trait of agronomical interest; it greatly influences the vineyard management and the visual aspect of table grape. Clusters with greater compactness are more susceptible to disease. The compactness can be break down in a patchwork of agronomical traits, each having agronomical importance that includes parameters related to inflorescence and cluster architecture (cluster length and width, length of pedicels, etc.), fruitfulness (number of berries, number of seeds) and berry (size, shape, volume...). Through visual evaluation of a collection of 730 clones from the cultivar Tempranillo and 501 clones from Garnacha Tinta we identified and fully phenotyped distinct clones which transcriptomes were compared at key developmental stages in order to identify the genes playing a role in mechanisms involved in cluster compactness such as the ones determining number of berries, cluster length or berry size. Key genes involved in this process were identified. The findings lead us to hypothesize that berry size and/or number at ripening are greatly influenced by the rate of cell replication in flowers during the first stages after pollination. A total of 57 samples were hybridized. Comparison G1 was performed between clones showing differences in the cluster compactness and in the total number of berries per cluster and berries size (compact: clone 1134. loose: clone 0368). Comparison G2 was performed between two compact clones (Garnacha Tinta 147 and 1134) significantly differing for cluster length and number of nodes (branches) of the rachis. Comparison G3 was performed with two loose clones (Garnacha Tinta 681 and 1154) differing in the number of nodes of the rachis (p<0.01). Comparisons G4 and T were performed between clones showing differences in the cluster compactness and in the total number of berries per cluster (compact: clones 0906 and 0126. loose: clones 1154 and 1041).

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Project description:Somatic mutations in ARID1A, a SWI/SNF chromatin remodeling gene, are prevalent in human malignancies linked to endometriosis. Through comprehensive chromatin immunoprecipitation sequencing and transposase-accessible chromatin sequencing, we identified chromatin binding regions for ARID1A/BRG1-containing SWI/SNF remodeling complexes, which were enriched at enhancers and corresponded to a euchromatin state. ARID1A deletion caused global affinity reduction of BRG1-containing complexes in chromatin. Integrative analyses with transcriptome data obtained from endometrial epithelium and human endometrioid carcinomas identified high-confidence ARID1A-regulated genes that participate in tissue regeneration and tumorigenesis. Deletion of Arid1a was found to inactivate the TGF-β pathway and to accelerate tumor progression from pre-cancerous lesions to endometrioid carcinomas. Collectively, this study establishes functional roles of ARID1A mutation and loss in tumor progression.

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Inactivation of ARID1A-SWI/SNF Complex Alters Chromatin Compactness at Enhancer Regions and Affects Transcription of Key Tumor Signaling Circuitry [ATAC-Seq]

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