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SWI/SNF component ARID1A restrains pancreatic neoplasia formation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE119859 | GEO | 2018/09/12

REPOSITORIES: GEO

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SWI/SNF component ARID1A restrains pancreatic neoplasia formation [RNA-seq]

Project description:ARID1A restrains the formation of PanIN, pancreas ductal adenocarcinoma, and intraductal mucinous neoplasms

2018-09-12 | GSE119779 | GEO

SWI/SNF component ARID1A restrains pancreatic neoplasia formation [ChIP-seq]

Project description:ARID1A restrains the formation of PanIN, pancreas ductal adenocarcinoma, and intraductal mucinous neoplasms

2018-09-12 | GSE119858 | GEO

SWI/SNF component ARID1A restrains pancreatic neoplasia formation

Project description:SWI/SNF component ARID1A restrains pancreatic neoplasia formation

| PRJNA490490 | ENA

SWI/SNF component ARID1A restrains pancreatic neoplasia formation [RNA-seq]

Project description:SWI/SNF component ARID1A restrains pancreatic neoplasia formation [RNA-seq]

| PRJNA490279 | ENA

SWI/SNF component ARID1A restrains pancreatic neoplasia formation [ChIP-seq]

Project description:SWI/SNF component ARID1A restrains pancreatic neoplasia formation [ChIP-seq]

| PRJNA490488 | ENA

Suppression of SWI/SNF component Arid1a promotes mammalian regeneration through chromatin remodeling

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-03-30 | E-GEOD-76935 | biostudies-arrayexpress

Suppression of the SWI/SNF Component Arid1a Promotes Mammalian Regeneration.

Project description:Mammals have partially lost the extensive regenerative capabilities of some vertebrates, possibly as a result of chromatin-remodeling mechanisms that enforce terminal differentiation. Here, we show that deleting the SWI/SNF component Arid1a substantially improves mammalian regeneration. Arid1a expression is suppressed in regenerating tissues, and genetic deletion of Arid1a increases tissue repair following an array of injuries. Arid1a deficiency in the liver increases proliferation, reduces tissue damage and fibrosis, and improves organ function following surgical resection and chemical injuries. Hepatocyte-specific deletion is also sufficient to increase proliferation and regeneration without excessive overgrowth, and global Arid1a disruption potentiates soft tissue healing in the ear. We show that Arid1a loss reprograms chromatin to restrict promoter access by transcription factors such as C/ebpα, which enforces differentiation, and E2F4, which suppresses cell-cycle re-entry. Thus, epigenetic reprogramming mediated by deletion of a single gene improves mammalian regeneration and suggests strategies to promote tissue repair after injury.

| S-EPMC4826298 | biostudies-literature

Suppression of SWI/SNF component Arid1a promotes mammalian regeneration through chromatin remodeling

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

2016-03-30 | GSE76935 | GEO

Downregulation of ARID1A, a component of the SWI/SNF chromatin remodeling complex, in breast cancer.

Project description:Recent studies unraveled that AT-rich interactive domain-containing protein 1A (ARID1A), a subunit of the mammary SWI/SNF chromatin remodeling complex, acts as a tumor suppressor in various cancers. In this study, we first evaluated ARID1A expression by immunohistochemistry in invasive breast cancer tissue specimens and assessed the correlation with the prognosis of patients with breast cancer. Non-tumorous mammary duct epithelial cells exhibited strong nuclear ARID1A staining, whereas different degrees of loss in ARID1A immunoreactivity were observed in many invasive breast cancer cells. We scored ARID1A immunoreactivity based on the sum of the percentage score in invasive cancer cells (on a scale of 0 to 5) and the intensity score (on a scale of 0 to 3), for a possible total score of 0 to 8. Interestingly, partial loss of ARID1A expression, score 2 to 3, was significantly correlated with poor disease free survival of the patients. Subsequently, we performed siRNA-mediated ARID1A knockdown in cultured breast cancer cells followed by comprehensive gene profiling and quantitative RT-PCR. Interestingly, many genes were downregulated by partial loss of ARID1A, whereas RAB11FIP1 gene expression was significantly upregulated by partial loss of ARID1A expression in breast cancer cells. In contrast, a more than 50% reduction in ARID1A mRNA decreased RAB11FIP1gene expression. Immunoblotting also demonstrated that partial downregulation of ARID1A mRNA at approximately 20% reduction significantly increased the expression of RAB11FIP1 protein in MCF-7 cells, whereas, over 50% reduction of ARID1A mRNA resulted in reduction of RAB11FIP1 protein in cultured breast cancer cells. Recent studies reveal that RAB11FIP1 overexpression leads to breast cancer progression. Altogether, the present findings indicated that partial loss of ARID1A expression is linked to unfavorable outcome for patients with breast cancer, possibly due to increased RAB11FIP1 expression.

| S-EPMC5264034 | biostudies-literature

ARID1A, a component of SWI/SNF chromatin remodeling complexes, is required for porcine embryo development.

Project description:Mammalian embryos undergo dramatic epigenetic remodeling that can have a profound impact on both gene transcription and overall embryo developmental competence. Members of the SWI/SNF (Switch/Sucrose non-fermentable) family of chromatin-remodeling complexes reposition nucleosomes and alter transcription factor accessibility. These large, multi-protein complexes possess an SNF2-type ATPase (either SMARCA4 or SMARCA2) as their core catalytic subunit, and are directed to specific loci by associated subunits. Little is known about the identity of specific SWI/SNF complexes that serve regulatory roles during cleavage development. ARID1A, one of the SWI/SNF complex subunits, can affect histone methylation in somatic cells; here, we determined the developmental requirements of ARID1A in porcine oocytes and embryos. We found ARID1A transcript levels were significantly reduced in 4-cell porcine embryos as compared to germinal vesicle-stage oocytes, suggesting that ARID1A would be required for porcine cleavage-stage development. Indeed, injecting in vitro-matured and fertilized porcine oocytes with double-stranded interfering RNAs that target ARID1A, and evaluating their phenotype after seven days, revealed that the depletion of ARID1A results in significantly fewer cells than their respective control groups (p < 0.001).

| S-EPMC5760285 | biostudies-literature

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