Arid1a is essential for endometrial gland development
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA564689 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Arid1a has a critical role for modulating endometrial gland develop that is required for normal uterine function and fertility after maturity. We used microarrays to detail the mechanism underlying Arid1a loss during postnatal development.
2019-11-06 | GSE137166 | GEO
Project description:Endometrial epithelial Arid1a is necessary for normal gene expression and maintenance of a receptive endometrium at pre-implantation stage in mice. We used RNA-sequencing to determine the differences in uterine gene expression resulting from deletion of endometrial epithelial Arid1a.
2022-03-01 | GSE196489 | GEO
Project description:Endometrial epithelial Arid1a is essential in early pregnancy
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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 | 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 | 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
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 | GSE148470 | 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