Gene-expression analysis of iEEC16 endometriosis cells with ARID1A KD
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE86572 | GEO | 2017/03/31
SECONDARY ACCESSION(S): PRJNA342266
REPOSITORIES: GEO
Similar Datasets
Project description:We show that knocking down ARID1A in an immortalized endometriosis cell line leads to phenotypic changes in vitro. Additionally, we find strong increases in the active H3K27ac mark in promoter regions but decrease of H3K27ac at potential enhancers with targeted DNA methylation-independent alterations in nucleosome occupancy.
2017-04-05 | GSE97373 | GEO
Project description:We show that knocking down ARID1A in an immortalized endometriosis cell line leads to phenotypic changes in vitro. Additionally, we find strong increases in the active H3K27ac mark in promoter regions but decrease of H3K27ac at potential enhancers.
2017-04-05 | GSE86810 | GEO
Project description:Illumina array was employed to analyze the genes whose expression are altered when ARID1A gene is downregulated by shRNA in normal ovarian surface epithelial cells OSE4 and IOSE80pc. This leads to discovery of p53-regulated genes such as p21 and SMAD3. ARID1A knockdown in OSE4 and IOSE80pc
2012-05-01 | E-GEOD-37684 | biostudies-arrayexpress
Project description:A nonsense mutation in ARID1A was identified by next generation sequencing in non-dysplastic Barrett's esophagus [BE] tissue and esophageal adenocarcinoma [EAC] tissue of a patient diagnosed with EAC. Immunohistochemistry performed on an independent archival cohort demonstrated ARID1A protein loss in 0% (0/76), 4.9% (2/40), 14.3% (4/28), 16.0% (8/50), and 12.2% (12/98) of normal squamous epithelium, BE, low-, high-grade dysplasia, and EAC tissues, respectively. Enhanced cell growth, proliferation and invasion were observed upon ARID1A knockdown in EAC cells. ARID1A was knocked down in OE33 cells (Sample MS_1 and MS_3) using on-TARGET smartpool ARID1A siRNA. At the same time, OE33 cells were transfected with a non-targeting siRNA, and these experiments (Samples MS_2 and MS_4) functioned as mock controls. Cells were harvested after 48 hours and total RNA was extracted using the Rneasy kit (Qiagen) Aim Affymetrix Human PrimeView Gene Expression Array : to determine the downstream effectors of ARID1A that are likely to contribute to the oncogenic phenotype caused by ARID1A down-regulation. Two biological replicates of each condition (2x ARID1A knockdown, and 2x Mock) were used for the microarray experiment.
2012-05-31 | E-GEOD-38380 | biostudies-arrayexpress
Project description:Endometriosis affects 1-in-10 women and is characterized by the presence of abnormal endometrium at ectopic sites. ARID1A mutations are observed in deeply invasive forms of the disease, often correlating with malignancy. To identify epigenetic dependencies driving invasion, we utilized an unbiased approach to map chromatin state transitions accompanying ARID1A loss in the endometrium. We show that super-enhancers marked by high H3K27-acetylation are strongly associated with ARID1A binding. ARID1A loss leads to H3K27-hyperacetylation and increased chromatin accessibility and enhancer RNA transcription at super-enhancers, but not typical enhancers, indicating that ARID1A normally prevents super-enhancer hyperactivation. ARID1A co-localizes with P300 at super-enhancers, and genetic or pharmacological inhibition of P300 in ARID1A-mutant endometrial epithelia suppresses invasion and induces anoikis through rescue of super-enhancer hyperacetylation. Among hyperactivated super-enhancers, SERPINE1 (PAI-1) was identified as an essential target gene driving ARID1A-mutant endometrial invasion. Broadly, our findings provide rationale for therapeutic strategies targeting super-enhancers in ARID1A-mutant endometrium.
2020-11-10 | GSE157735 | GEO
Project description:Endometriosis affects 1-in-10 women and is characterized by the presence of abnormal endometrium at ectopic sites. ARID1A mutations are observed in deeply invasive forms of the disease, often correlating with malignancy. To identify epigenetic dependencies driving invasion, we utilized an unbiased approach to map chromatin state transitions accompanying ARID1A loss in the endometrium. We show that super-enhancers marked by high H3K27-acetylation are strongly associated with ARID1A binding. ARID1A loss leads to H3K27-hyperacetylation and increased chromatin accessibility and enhancer RNA transcription at super-enhancers, but not typical enhancers, indicating that ARID1A normally prevents super-enhancer hyperactivation. ARID1A co-localizes with P300 at super-enhancers, and genetic or pharmacological inhibition of P300 in ARID1A-mutant endometrial epithelia suppresses invasion and induces anoikis through rescue of super-enhancer hyperacetylation. Among hyperactivated super-enhancers, SERPINE1 (PAI-1) was identified as an essential target gene driving ARID1A-mutant endometrial invasion. Broadly, our findings provide rationale for therapeutic strategies targeting super-enhancers in ARID1A-mutant endometrium.
2020-11-10 | GSE157732 | GEO
Project description:Endometriosis affects 1-in-10 women and is characterized by the presence of abnormal endometrium at ectopic sites. ARID1A mutations are observed in deeply invasive forms of the disease, often correlating with malignancy. To identify epigenetic dependencies driving invasion, we utilized an unbiased approach to map chromatin state transitions accompanying ARID1A loss in the endometrium. We show that super-enhancers marked by high H3K27-acetylation are strongly associated with ARID1A binding. ARID1A loss leads to H3K27-hyperacetylation and increased chromatin accessibility and enhancer RNA transcription at super-enhancers, but not typical enhancers, indicating that ARID1A normally prevents super-enhancer hyperactivation. ARID1A co-localizes with P300 at super-enhancers, and genetic or pharmacological inhibition of P300 in ARID1A-mutant endometrial epithelia suppresses invasion and induces anoikis through rescue of super-enhancer hyperacetylation. Among hyperactivated super-enhancers, SERPINE1 (PAI-1) was identified as an essential target gene driving ARID1A-mutant endometrial invasion. Broadly, our findings provide rationale for therapeutic strategies targeting super-enhancers in ARID1A-mutant endometrium.
2020-11-10 | GSE157731 | GEO
Project description:Endometriosis affects 1-in-10 women and is characterized by the presence of abnormal endometrium at ectopic sites. ARID1A mutations are observed in deeply invasive forms of the disease, often correlating with malignancy. To identify epigenetic dependencies driving invasion, we utilized an unbiased approach to map chromatin state transitions accompanying ARID1A loss in the endometrium. We show that super-enhancers marked by high H3K27-acetylation are strongly associated with ARID1A binding. ARID1A loss leads to H3K27-hyperacetylation and increased chromatin accessibility and enhancer RNA transcription at super-enhancers, but not typical enhancers, indicating that ARID1A normally prevents super-enhancer hyperactivation. ARID1A co-localizes with P300 at super-enhancers, and genetic or pharmacological inhibition of P300 in ARID1A-mutant endometrial epithelia suppresses invasion and induces anoikis through rescue of super-enhancer hyperacetylation. Among hyperactivated super-enhancers, SERPINE1 (PAI-1) was identified as an essential target gene driving ARID1A-mutant endometrial invasion. Broadly, our findings provide rationale for therapeutic strategies targeting super-enhancers in ARID1A-mutant endometrium.
2020-11-10 | GSE148473 | GEO
Project description:Endometriosis affects 1-in-10 women and is characterized by the presence of abnormal endometrium at ectopic sites. ARID1A mutations are observed in deeply invasive forms of the disease, often correlating with malignancy. To identify epigenetic dependencies driving invasion, we utilized an unbiased approach to map chromatin state transitions accompanying ARID1A loss in the endometrium. We show that super-enhancers marked by high H3K27-acetylation are strongly associated with ARID1A binding. ARID1A loss leads to H3K27-hyperacetylation and increased chromatin accessibility and enhancer RNA transcription at super-enhancers, but not typical enhancers, indicating that ARID1A normally prevents super-enhancer hyperactivation. ARID1A co-localizes with P300 at super-enhancers, and genetic or pharmacological inhibition of P300 in ARID1A-mutant endometrial epithelia suppresses invasion and induces anoikis through rescue of super-enhancer hyperacetylation. Among hyperactivated super-enhancers, SERPINE1 (PAI-1) was identified as an essential target gene driving ARID1A-mutant endometrial invasion. Broadly, our findings provide rationale for therapeutic strategies targeting super-enhancers in ARID1A-mutant endometrium.
2020-11-10 | GSE148472 | GEO
Project description:Endometriosis affects 1-in-10 women and is characterized by the presence of abnormal endometrium at ectopic sites. ARID1A mutations are observed in deeply invasive forms of the disease, often correlating with malignancy. To identify epigenetic dependencies driving invasion, we utilized an unbiased approach to map chromatin state transitions accompanying ARID1A loss in the endometrium. We show that super-enhancers marked by high H3K27-acetylation are strongly associated with ARID1A binding. ARID1A loss leads to H3K27-hyperacetylation and increased chromatin accessibility and enhancer RNA transcription at super-enhancers, but not typical enhancers, indicating that ARID1A normally prevents super-enhancer hyperactivation. ARID1A co-localizes with P300 at super-enhancers, and genetic or pharmacological inhibition of P300 in ARID1A-mutant endometrial epithelia suppresses invasion and induces anoikis through rescue of super-enhancer hyperacetylation. Among hyperactivated super-enhancers, SERPINE1 (PAI-1) was identified as an essential target gene driving ARID1A-mutant endometrial invasion. Broadly, our findings provide rationale for therapeutic strategies targeting super-enhancers in ARID1A-mutant endometrium.
2020-11-10 | GSE148471 | GEO