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Uncovering the dosage-dependent roles of Arid1a in gastric tumorigenesis for combinatorial drug therapy

ABSTRACT: Uncovering the dosage-dependent roles of Arid1a in gastric tumorigenesis for combinatorial drug therapy

PROVIDER: PRJNA603539 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10981147.fastq.gz	Fastqsanger.gz
	SRR10981148.fastq.gz	Fastqsanger.gz
	SRR10981149.fastq.gz	Fastqsanger.gz
	SRR10981150.fastq.gz	Fastqsanger.gz
	SRR10981151.fastq.gz	Fastqsanger.gz

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Uncovering the dosage-dependent roles of Arid1a in gastric tumorigenesis for combinatorial drug therapy [scRNA-Seq]

Project description:Gastric cancer (GC) is one of the most common deadly cancers in the world. Although patient genomic data have identified ARID1A, a key chromatin remodeling complex subunit, as the second most frequently mutated gene after TP53, its in vivo role and relationship to TP53 in gastric tumorigenesis remains unclear. Establishing a novel mouse model that reflects the ARID1A heterozygous mutations found in the majority of human GC cases, we demonstrated that Arid1a heterozygosity facilitates tumor progression through a global loss of enhancers and subsequent suppression of the p53 and apoptosis pathways. Moreover, our mouse genetic and single cell analyses demonstrated that the homozygous deletion of Arid1a confers a competitive disadvantage through the activation of the p53 pathway, highlighting its distinct dosage dependent roles. Utilizing this unique vulnerability of Arid1a mutated GC cells, our combinatorial treatment with an epigenetic inhibitor and a p53 agonist selectively inhibited Arid1a heterozygous tumor growth, providing a novel therapeutic option for GC.

2021-03-16 | GSE144387 | GEO

Uncovering the dosage-dependent roles of Arid1a in gastric tumorigenesis for combinatorial drug therapy [RNA-Seq]

2021-03-16 | GSE144386 | GEO

Uncovering the dosage-dependent roles of Arid1a in gastric tumorigenesis for combinatorial drug therapy [ChIP-Seq]

2021-03-16 | GSE144385 | GEO

Uncovering the dosage-dependent roles of Arid1a in gastric tumorigenesis for combinatorial drug therapy [RNA-Seq]

Project description:Uncovering the dosage-dependent roles of Arid1a in gastric tumorigenesis for combinatorial drug therapy [RNA-Seq]

| PRJNA603540 | ENA

Uncovering the dosage-dependent roles of Arid1a in gastric tumorigenesis for combinatorial drug therapy [ChIP-Seq]

Project description:Uncovering the dosage-dependent roles of Arid1a in gastric tumorigenesis for combinatorial drug therapy [ChIP-Seq]

| PRJNA603541 | ENA

Uncovering the dosage-dependent roles of Arid1a in gastric tumorigenesis for combinatorial drug therapy [scRNA-Seq]

Project description:Uncovering the dosage-dependent roles of Arid1a in gastric tumorigenesis for combinatorial drug therapy [scRNA-Seq]

| PRJNA603542 | ENA

Uncovering the dosage-dependent roles of Arid1a in gastric tumorigenesis for combinatorial drug therapy.

Project description:Gastric cancer (GC) is one of the most common deadly cancers in the world. Although patient genomic data have identified AT-rich interaction domain 1A (ARID1A), a key chromatin remodeling complex subunit, as the second most frequently mutated gene after TP53, its in vivo role and relationship to TP53 in gastric tumorigenesis remains unclear. Establishing a novel mouse model that reflects the ARID1A heterozygous mutations found in the majority of human GC cases, we demonstrated that Arid1a heterozygosity facilitates tumor progression through a global loss of enhancers and subsequent suppression of the p53 and apoptosis pathways. Moreover, mouse genetic and single-cell analyses demonstrated that the homozygous deletion of Arid1a confers a competitive disadvantage through the activation of the p53 pathway, highlighting its distinct dosage-dependent roles. Using this unique vulnerability of Arid1a mutated GC cells, our combined treatment with the epigenetic inhibitor, TP064, and the p53 agonist, Nutlin-3, inhibited growth of Arid1a heterozygous tumor organoids, providing a novel therapeutic option for GC.

| S-EPMC8034383 | biostudies-literature

Uncovering the dosage-dependent roles of Arid1a in gastric tumorigenesis for combinatorial drug therapy

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

2021-03-16 | GSE144388 | GEO

Arid1a deletion in collaboration with Pten deletion leads to ovarian tumorigenesis in mouse

Project description:Mice developed ovarian tumors after Arid1a and Pten double knockout. Gene expression profiles of 5 such ovarian tumors were compared with those of 4 normal ovaries. The differentially expressed genes were then used to investigate the similarity between the mouse ovarian tumors and major subtypes of human ovarian cancers. Total RNA obtained from the mouse ovarian tumors developing after Arid1a and Pten knockout compared to normal mouse ovaries.

2014-04-05 | E-GEOD-56531 | biostudies-arrayexpress

Co-existing TP53 and ARID1A mutations promote aggressive endometrial tumorigenesis [CUT&RUN]

Project description:TP53 and ARID1A are frequently mutated across cancer but rarely in the same primary tumor. Endometrial cancer has the highest TP53-ARID1A mutual exclusivity rate. However, the functional relationship between TP53 and ARID1A mutations in the endometrium has not been elucidated. We used genetically engineered mice and in vivo genomic approaches to discern both unique and overlapping roles of TP53 and ARID1A in the endometrium. TP53 loss with oncogenic PIK3CA*H1047R in the endometrial epithelium results in features of endometrial hyperplasia, adenocarcinoma, and intraepithelial carcinoma. Mutant endometrial epithelial cells were transcriptome profiled and compared to control cells and ARID1A/PIK3CA mutant endometrium. In the context of either TP53 or ARID1A loss, PIK3CA mutant endometrium exhibited inflammatory pathway activation, but other gene expression programs differed based on TP53 or ARID1A status, such as epithelial-to-mesenchymal transition. Gene expression patterns observed in the genetic mouse models are reflective of human tumors with each respective genetic alteration. Consistent with TP53-ARID1A mutual exclusivity, the p53 pathway is activated following ARID1A loss in the endometrial epithelium, where ARID1A normally directly represses p53 pathway genes in vivo, including the stress-inducible transcription factor, ATF3. However, co-existing TP53-ARID1A mutations led to invasive adenocarcinoma associated with mutant ARID1A-driven ATF3 induction, reduced apoptosis, TP63+ squamous differentiation and invasion. These data suggest TP53 and ARID1A mutations drive shared and distinct tumorigenic programs in the endometrium and promote invasive endometrial cancer when existing simultaneously. Hence, TP53 and ARID1A mutations may co-occur in a subset of aggressive or metastatic endometrial cancers, with ARID1A loss promoting squamous differentiation and the acquisition of invasive properties.

2021-12-13 | GSE184498 | GEO

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