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Aberrant upregulation of RUNX3 activates developmental genes to drive metastasis in gastric cancer (ChIP-seq)

ABSTRACT: Aberrant upregulation of RUNX3 activates developmental genes to drive metastasis in gastric cancer (ChIP-seq)

PROVIDER: PRJNA1054140 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27277500.fastq.gz	Fastqsanger.gz
	SRR27277501.fastq.gz	Fastqsanger.gz
	SRR27277502.fastq.gz	Fastqsanger.gz
	SRR27277503.fastq.gz	Fastqsanger.gz
	SRR27277504.fastq.gz	Fastqsanger.gz

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Similar Datasets

Aberrant upregulation of RUNX3 activates developmental genes to drive metastasis in gastric cancer.

Project description:Aberrant upregulation of RUNX3 activates developmental genes to drive metastasis in gastric cancer.

| PRJNA1054135 | ENA

Aberrant upregulation of RUNX3 activates developmental genes to drive metastasis in gastric cancer (HiChIP)

Project description:Aberrant upregulation of RUNX3 activates developmental genes to drive metastasis in gastric cancer (HiChIP)

| PRJNA1054139 | ENA

Aberrant upregulation of RUNX3 activates developmental genes to drive metastasis in gastric cancer (HiChIP)

Project description:Gastric cancer metastasis is a major cause of mortality worldwide. Inhibition of RUNX3 in gastric cancer cell lines reduced migration, invasion, and anchorage independent growth in vitro. Following splenic inoculation, CRISPR-mediated RUNX3-knockout HGC-27 cells show suppression of xenograft growth and liver metastasis. We interrogated the potential of RUNX3 as a metastasis driver in gastric cancer by profiling its target genes. Transcriptomic analysis revealed strong involvement of RUNX3 in the regulation of multiple developmental pathways, consistent with the notion that RUNX family genes are master regulators of development. RUNX3 promoted “cell migration” and “extracellular matrix” programs, which are necessary for metastasis. Of note, we found pro-metastatic genes WNT5A, CD44 and VIM among the top differentially expressed genes in RUNX3-knockout versus control cells. Chromatin immunoprecipitation sequencing and HiChIP analyses revealed that RUNX3 bound to the enhancers and promoters of these genes, suggesting that they are under direct transcriptional control by RUNX3. We show that RUNX3 promoted metastasis in part through its upregulation of WNT5A to promote migration, invasion, and anchorage-independent growth in various malignancies. Our study therefore reveals the RUNX3-WNT5A axis as a key targetable mechanism for gastric cancer metastasis.

2023-12-20 | GSE250480 | GEO

Aberrant upregulation of RUNX3 activates developmental genes to drive metastasis in gastric cancer (RNA-seq)

Project description:Aberrant upregulation of RUNX3 activates developmental genes to drive metastasis in gastric cancer (RNA-seq)

| PRJNA1052672 | ENA

Aberrant upregulation of RUNX3 activates developmental genes to drive metastasis in gastric cancer (ChIP-seq)

2023-12-20 | GSE250479 | GEO

Aberrant upregulation of RUNX3 activates developmental genes to drive metastasis in gastric cancer (RNA-seq)

2023-12-20 | GSE250207 | GEO

Aberrant upregulation of RUNX3 activates developmental genes to drive metastasis in gastric cancer.

Project description:Gastric cancer metastasis is a major cause of mortality worldwide. Inhibition of RUNX3 in gastric cancer cell lines reduced migration, invasion, and anchorage independent growth in vitro. Following splenic inoculation, CRISPR-mediated RUNX3-knockout HGC-27 cells show suppression of xenograft growth and liver metastasis. We interrogated the potential of RUNX3 as a metastasis driver in gastric cancer by profiling its target genes. Transcriptomic analysis revealed strong involvement of RUNX3 in the regulation of multiple developmental pathways, consistent with the notion that RUNX family genes are master regulators of development. RUNX3 promoted "cell migration" and "extracellular matrix" programs, which are necessary for metastasis. Of note, we found pro-metastatic genes WNT5A, CD44 and VIM among the top differentially expressed genes in RUNX3-knockout versus control cells. Chromatin immunoprecipitation sequencing and HiChIP analyses revealed that RUNX3 bound to the enhancers and promoters of these genes, suggesting that they are under direct transcriptional control by RUNX3. We show that RUNX3 promoted metastasis in part through its upregulation of WNT5A to promote migration, invasion, and anchorage-independent growth in various malignancies. Our study therefore reveals the RUNX3-WNT5A axis as a key targetable mechanism for gastric cancer metastasis.

| S-EPMC10836196 | biostudies-literature

Aberrant upregulation of RUNX3 activates developmental genes to drive metastasis in gastric cancer.

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

2023-12-20 | GSE250481 | GEO

KSN01_Proteome_CellLine: Aberrant (pro)renin receptor expression induces genomic instability in pancreatic ductal adenocarcinoma through upregulation of SMARCA5/SNF2H

Project description:Aberrant (pro)renin receptor expression induces genomic instability in pancreatic ductal adenocarcinoma through upregulation of SMARCA5/SNF2H

2020-12-15 | PXD010107 | JPOST Repository

Runx3 pioneers chromatin accessibility of cis-regulatory landscapes that drive memory CTL formation

Project description:T cell receptor (TCR) stimulation of naïve CD8+ T cells initiates reprogramming of cis-regulatory landscapes that specify effector and memory cytotoxic T lymphocyte (CTL) differentiation. We mapped regions of hyper-accessible chromatin in naïve cells during TCR stimulation and discovered that the transcription factor (TF) Runx3 controls de novo access to memory CTL-specific cistromes prior to the first cell division, and is essential for memory CTL differentiation. Runx3 specifically promotes accessibility of cis-acting regions highly enriched with IRF, bZIP and Prdm1-like family TF motifs, upregulates IRF4 and establishes feed-forward transcriptional circuits that induce fundamental CTL attributes in memory precursor cells. Runx3 drives uncoupling from the naïve cell state, but subsequently restrains terminal differentiation of nascent CTL by preventing high expression of the TF T-bet and slowing effector cell proliferation. Enforced Runx3 expression enhances memory CTL differentiation and increases their numbers during iterative infections. Thus, Runx3 functions in a pioneering role to initialize and then ensure memory CTL differentiate. This SuperSeries is composed of the SubSeries listed below.

2018-04-19 | GSE111149 | GEO

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