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

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

PROVIDER: PRJNA603542 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10981164.fastq.gz	Fastqsanger.gz
	SRR10981165.fastq.gz	Fastqsanger.gz
	SRR10981166.fastq.gz	Fastqsanger.gz
	SRR10981167.fastq.gz	Fastqsanger.gz
	SRR10981168.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

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

| PRJNA603539 | ENA

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

2021-03-16 | GSE144387 | GEO

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 [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.

Project description: Not available

| 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

Gene dosage imbalance contributes to chromosomal instability-induced tumorigenesis

Project description:Chromosomal instability (CIN) is thought to be a source of mutability in human cancer. However, CIN is highly deleterious for the cell, and the resulting aneuploidy induces metabolic stress and compromises cell fitness. Here we utilized the X-chromosome dosage compensation mechanism and changes in X-chromosome number to demonstrate in Drosophila epithelial cells the causal relationship between CIN, aneuploidy, gene dosage imbalance and tumorigenesis. Whereas the harmful effects of CIN can be buffered by resetting the X-chromosome dosage compensation to compensate for changes in X-chromosome number, interfering with the mechanisms of dosage compensation suffices to induce tumorigenesis. In addition, multiple mechanisms buffer the deleterious effects of CIN including DNA-damage repair, activation of the p38 signalling pathway, and induction of cytokine expression to promote compensatory cell proliferation. These data reveal a key role of gene dosage imbalances to CIN-induced programmed cell death and tumorigenesis and the existence of robust compensatory mechanisms.

2016-05-23 | GSE71242 | 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

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