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

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

PROVIDER: PRJNA1054139 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27277572_1.fastq.gz	Fastqsanger.gz
	SRR27277572_2.fastq.gz	Fastqsanger.gz

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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.

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 (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 (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)

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

| PRJNA1054140 | ENA

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

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

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

The interactomes of RUNX1 and RUNX3 from Mus musculus T cells

Project description:Cellular binary fate decisions require the progeny to silence genes associated with the alternative fate. The major subsets of alpha:beta T cells have been extensively studied as a model system for fate decisions. While the transcription factor RUNX3 is required for the initiation of Cd4 silencing in CD8 T cell progenitors, it is not required to maintain the silencing of Cd4 and other helper T lineage genes. The other runt domain containing protein, RUNX1, silences Cd4 in an earlier T cell progenitor, but this silencing is reversed whereas the gene silencing after RUNX3 expression is not reverse. Therefore, we hypothesized that RUNX3 and not RUNX1 recruits other factors that maintains the silencing of helper T lineage genes in CD8 T cells. To this end, we performed a proteomics screen of RUNX1 and RUNX3 to determine candidate silencing factors.

2019-11-12 | PXD007511 | Pride

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