GEO DataSets

(Submitter supplied) ARID1A, encoding a subunit of the SWI/SNF chromatin remodeling complex, is the most mutated epigenetic regulator in human cancers. ARID1A and TP53 mutations are typically mutually exclusive. Therapeutic approaches that correlate with ARID1A mutational status remain a challenge. Here, we show that HDAC6 activity is essential in ARID1A-mutated ovarian cancers. Inhibition of HDAC6 activity using a clinically applicable small molecule inhibitor significantly improved the survival of mice bearing ARID1A-mutated ovarian tumors. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

5 Samples

Download data: TXT

(Submitter supplied) xenograft, patientderived xenograft and the genetic Arid1aflox/flox/Pik3caH1047R mouse models. Finally, B-I09 synergizes with inhibition of HDAC6, a known regulator of the ER stress response, in suppressing the growth of ARID1A-inactivated OCCCs. These studies reveal a promising therapeutic strategy for ARID1A-mutant OCCCs and define the IRE1?-XBP1 axis of the ER stress response as a targetable vulnerability for ARID1A-mutant OCCCs. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

12 Samples

Download data: TXT

(Submitter supplied) ARID1A, encoding a subunit of the SWI/SNF chromatin remodeling complex, is the most frequently mutated epigenetic regulators in human cancers. ARID1A is mutated in over 50% ovarian clear cell carcinoma, a disease currently has no effective therapy. Here we show that ARID1A-mutated ovarian cancer cells are selectively sensitive to inhibition of HDAC2 activity. HDAC2 interacts with EZH2 in an ARID1A status dependent manner. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

3 Samples

Download data: TXT

(Submitter supplied) ARID1A is frequently mutated in ovarian clear-cell carcinoma (OCCC) and often co-exists with activating mutations of PIK3CA. Although induction of pro-inflammatory cytokines has been observed in this cancer, the mechanism by which the two mutations synergistically activate cytokine genes remains elusive. Here we established an in vitro model of OCCC by introducing ARID1A knock-down and mutant PIK3CA in a normal human ovarian epithelial cell line, which resulted in cell transformation and cytokine gene induction. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL16791

12 Samples

Download data: XLSX

(Submitter supplied) 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.

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS4826

Platform:

GPL10558

4 Samples

Download data: TXT

Analysis of OSE4 and IOSE80pc ovarian surface epithelial cells depleted for ARID1A, which encodes large nuclear protein p270. ARID1A depletion enhances OSE4 and IOSE80pc proliferation. OSE4 cells become highly tumorigenic upon ARID1A depletion. Results suggest a tumor-suppressor role for ARID1A.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 2 cell line, 2 protocol sets

Platform:

GPL10558

Series:

GSE37684

4 Samples

Download data

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing

Platform:

GPL18573

7 Samples

Download data: TXT

(Submitter supplied) The SWI/SNF chromatin remodeling complex is altered in ~20% of human cancers. ARID1A, a component of the SWI/SNF chromatin-remodeling complex, is the most frequently mutated epigenetic regulator in human cancers. Inactivation of the SWI/SNF complex is synthetically lethal with inhibition of EZH2 activity. EZH2 inhibitors are entering clinical trials for specific tumor types with SWI/SNF mutations. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

5 Samples

Download data: TXT

(Submitter supplied) The SWI/SNF chromatin remodeling complex is altered in ~20% of human cancers. ARID1A, a component of the SWI/SNF chromatin-remodeling complex, is the most frequently mutated epigenetic regulator in human cancers. Inactivation of the SWI/SNF complex is synthetically lethal with inhibition of EZH2 activity. EZH2 inhibitors are entering clinical trials for specific tumor types with SWI/SNF mutations. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL18573

2 Samples

Download data: TXT

(Submitter supplied) We investigated the genomic consequences of the depletion of the SWI/SNF subumit ARID1A, in an ovarian cancer derived model. We produced genome wide data for nascent RNA (GRO-seq) and steady state RNA (total RNA-seq). Further, we used ChIP-seq to examine genome-wide distribution of ARID1A, as well as the changes in occupancy of RNAPII, H3K4me3 and H3K36me3. Finally we used ATAC-seq to investigate chromatin accessibility.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other

Platform:

GPL18573

37 Samples

Download data: BW, TXT

(Submitter supplied) ARID1A, an epigentic modifier, is often mutated in ovarian clear cell carcinoma (OCCC). In addition, EZH2 is frequently upregulated in OCCC. Inhibtion of EZH2 with an inhibitor (GSK126) selectively inhibits ARID1A-mutated cells. This study was designed to understand changes in gene expression profiles following EZH2 inhibition or ARID1A restoration.

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS5816

Platform:

GPL10558

9 Samples

Download data: TXT

Analysis of ARID1A-mutated OVISE ovarian clear cell carcinoma (OCCC) cells restored with wild-type ARID1A or treated with GSK126, an inhibitor of epigenetic regulator EZH2. Epigenetic modifier ARID1A is often mutated in OCCC. Results provide insight into the role of epigenetic mechanisms in OCCC.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 3 genotype/variation sets

Platform:

GPL10558

Series:

GSE54979

9 Samples

Download data

(Submitter supplied) To explore the sensitivity of ARID1A-KO cells to APR-246

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL13607

7 Samples

Download data: TXT

(Submitter supplied) ChIP-seq. analysis of TCam-2 16 h after 10 nanomolar Romidepsin application. DMSO treated cells were used as controls. For ChIP, an antibody against histone H3 pan-acetylation was used. These data are part of the article 'The Histone Deacetylase Inhibitor Romidepsin Efficiently Targets Cisplatin-resistant Germ Cell Cancer Cells via Downregulation of the SWI/SNF-Complex Member ARID1A' (Nettersheim et al., 2016).

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL18573

3 Samples

Download data: TXT

(Submitter supplied) Illumina 450k DNA methylation microarray analysis of TCam-2, 2102EP, NCCIT and JAR cells 16 h after 10 nanomolar Romidepsin application. DMSO treated cells were used as controls. These data are part of the article 'The Histone Deacetylase Inhibitor Romidepsin is a Novel Therapeutic Option for (Cisplatin-resistant) Germ Cell Cancers' (Nettersheim et al., 2016).

Organism:

Homo sapiens

Type:

Methylation profiling by array

Platform:

GPL13534

8 Samples

Download data: IDAT, TXT

(Submitter supplied) Illumina expression microarray analysis of TCam-2, 2102EP, NCCIT, JAR, MPAF, ARZ and FS1 cells 8 and 16 h after 10 nanomolar romidepsin application. DMSO treated cells were used as controls. These data are part of the article 'A signaling cascade including ARID1A, GADD45B and DUSP1 induces apoptosis and affects the cell cycle of germ cell cancers after romidepsin treatment' (Nettersheim et al., 2016).

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

28 Samples

Download data: TXT

(Submitter supplied) Ovarian clear cell carcinoma (OCCC) is an aggressive form of ovarian cancer with high ARID1A mutation rates. Here we present a genetically engineered mouse model of OCCC. We find that ARID1A inactivation is not sufficient for tumor formation, but requires concurrent activation of the phosphoinositide 3-kinase catalytic subunit, PIK3CA. Remarkably, the mice develop highly penetrant tumors with OCCC-like histopathology, culminating in hemorrhagic ascites and a median survival period of 7.5 weeks. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL17400

18 Samples

Download data: CEL

(Submitter supplied) We konckdown ARID1A and then detected differentially expressed genes

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL21185

6 Samples

Download data: TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing

Platform:

GPL20301

8 Samples

Download data: TXT

(Submitter supplied) mTORC1 is a conserved central controller of cell growth, which is commonly activated in hepatocellular carcinoma (HCC), driving liver tumorigenesis. In addition to its established cytoplasmic functions, mTORC1 is found in the nucleus where it regulates transcription by all three major RNA polymerases. However, precisely how mTORC1 controls gene expression remains poorly understood. Herein we show that mTORC1 interacts with the BAF SWI/SNF complex and regulates genome-wide chromatin remodeling through ARID1A. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20301

4 Samples

Download data: TXT