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SAMD1 suppresses epithelial-mesenchymal transition pathways in pancreatic ductal adenocarcinoma [ChIP-Seq]

ABSTRACT: SAMD1 suppresses epithelial-mesenchymal transition pathways in pancreatic ductal adenocarcinoma [ChIP-Seq]

PROVIDER: PRJNA999242 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25439830.fastq.gz	Fastqsanger.gz
	SRR25439831.fastq.gz	Fastqsanger.gz
	SRR25439832.fastq.gz	Fastqsanger.gz
	SRR25439833.fastq.gz	Fastqsanger.gz
	SRR26459769.fastq.gz	Fastqsanger.gz

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SAMD1 suppresses epithelial-mesenchymal transition pathways in pancreatic ductal adenocarcinoma

Project description:SAMD1 suppresses epithelial-mesenchymal transition pathways in pancreatic ductal adenocarcinoma

| PRJNA999235 | ENA

SAMD1 suppresses epithelial-mesenchymal transition pathways in pancreatic ductal adenocarcinoma [ChIP-Seq]

Project description:Pancreatic ductal adenocarcinoma (PDAC) poses a significant threat due to its tendency to evade early detection, frequent metastasis, and the subsequent challenges in devising effective treatments. Processes that govern epithelial-mesenchymal transition (EMT) in PDAC hold promise for advancing novel therapeutic strategies. SAMD1 (SAM domain-containing protein 1) is a CpG island-binding protein that plays a pivotal role in the repression of its target genes. Here, we revealed that SAMD1 acts as a repressor of genes associated with epithelial-mesenchymal transition (EMT). Upon deletion of SAMD1 in PDAC cells, we observed significantly increased migration rates. SAMD1 exerts its effects by binding to specific genomic targets, including CDH2, encoding N-cadherin, which emerged as a driver of enhanced migration upon SAMD1 knockout. Furthermore, we discovered the FBXO11-containing E3 ubiquitin ligase complex as an interactor and negative regulator of SAMD1, which inhibits SAMD1 chromatin binding genome-wide. High FBXO11 expression in PDAC is associated with poor prognosis and increased expression of EMT-related genes, underlining an antagonistic relationship between SAMD1 and FBXO11. In summary, our findings provide insights into the regulation of EMT-related genes in PDAC, shedding light on the intricate role of SAMD1 and its interplay with FBXO11 in this cancer type.

2024-06-27 | GSE239415 | GEO

SAMD1 suppresses epithelial-mesenchymal transition pathways in pancreatic ductal adenocarcinoma [RNA-Seq]

2024-06-27 | GSE239414 | GEO

SAMD1 suppresses epithelial-mesenchymal transition (EMT) in pancreatic ductal adenocarcinoma.

Project description:SAMD1, a CpG island-binding protein, plays a pivotal role in the repression of its target genes by influencing the activity of KDM1A. Despite its significant correlation with outcomes in various tumor types, SAMD1's role in cancer has remained largely unexplored. In this study, we focus on pancreatic ductal adenocarcinoma (PDAC) and reveal that SAMD1 is a repressor of genes associated with epithelial-mesenchymal transition (EMT). Upon depletion of SAMD1 in PDAC cells, we observed significantly increased migration rates. Furthermore, high SAMD1 expression in PDAC patients correlated with lower expression of EMT signature genes and better prognosis, further underscoring its suppressive role. In-depth analysis revealed that SAMD1 exerts its effects by binding to specific genomic targets, including CDH2, encoding N-Cadherin, which emerged as a driver of enhanced migration upon SAMD1 knockout. Our investigations further demonstrated reduced chromatin-binding activity of SAMD1 in PDAC cells, prompting a search for regulatory mechanisms. This led to the discovery of the FBXO11-containing E3 ubiquitin ligase complex as a novel interactor of SAMD1, critically influencing its chromatin binding genome-wide. High FBXO11 expression in PDAC is associated with poor prognosis and increased expression of EMT-related genes, implying an antagonistic relationship between SAMD1 and FBXO11. In summary, our findings provide new insights into the regulation of EMT-related genes in PDAC, shedding light on the intricate role of SAMD1 and its interplay with FBXO11 in this particular cancer type.

2024-07-12 | PXD044104 | Pride

SAMD1 suppresses epithelial-mesenchymal transition pathways in pancreatic ductal adenocarcinoma [RNA-Seq]

Project description:SAMD1 suppresses epithelial-mesenchymal transition pathways in pancreatic ductal adenocarcinoma [RNA-Seq]

| PRJNA999243 | ENA

SAMD1 suppresses epithelial-mesenchymal transition pathways in pancreatic ductal adenocarcinoma.

Project description:Pancreatic ductal adenocarcinoma (PDAC) poses a significant threat due to its tendency to evade early detection, frequent metastasis, and the subsequent challenges in devising effective treatments. Processes that govern epithelial-mesenchymal transition (EMT) in PDAC hold promise for advancing novel therapeutic strategies. SAMD1 (SAM domain-containing protein 1) is a CpG island-binding protein that plays a pivotal role in the repression of its target genes. Here, we revealed that SAMD1 acts as a repressor of genes associated with EMT. Upon deletion of SAMD1 in PDAC cells, we observed significantly increased migration rates. SAMD1 exerts its effects by binding to specific genomic targets, including CDH2, encoding N-cadherin, which emerged as a driver of enhanced migration upon SAMD1 knockout. Furthermore, we discovered the FBXO11-containing E3 ubiquitin ligase complex as an interactor and negative regulator of SAMD1, which inhibits SAMD1 chromatin-binding genome-wide. High FBXO11 expression in PDAC is associated with poor prognosis and increased expression of EMT-related genes, underlining an antagonistic relationship between SAMD1 and FBXO11. In summary, our findings provide insights into the regulation of EMT-related genes in PDAC, shedding light on the intricate role of SAMD1 and its interplay with FBXO11 in this cancer type.

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SAMD1 suppresses epithelial-mesenchymal transition pathways in pancreatic ductal adenocarcinoma

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

2024-06-27 | GSE239418 | GEO

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