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Cell differentiation grade determines distinct FOXA2 contributions to the cis-regulatory networks of pancreatic cancer cells [RNA-seq]

ABSTRACT: Cell differentiation grade determines distinct FOXA2 contributions to the cis-regulatory networks of pancreatic cancer cells [RNA-seq]

PROVIDER: PRJNA490732 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7826340.fastq.gz	Fastqsanger.gz
	SRR7826350.fastq.gz	Fastqsanger.gz
	SRR7826341.fastq.gz	Fastqsanger.gz
	SRR7826351.fastq.gz	Fastqsanger.gz
	SRR7826342.fastq.gz	Fastqsanger.gz

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Cell differentiation grade determines distinct FOXA2 contributions to the cis-regulatory networks of pancreatic cancer cells

Project description:Cell differentiation grade determines distinct FOXA2 contributions to the cis-regulatory networks of pancreatic cancer cells

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Cell differentiation grade determines distinct FOXA2 contributions to the cis-regulatory networks of pancreatic cancer cells [ChIP-seq]

Project description:Cell differentiation grade determines distinct FOXA2 contributions to the cis-regulatory networks of pancreatic cancer cells [ChIP-seq]

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Cell differentiation grade determines distinct FOXA2 contributions to the cis-regulatory networks of pancreatic cancer cells [ATAC-seq]

Project description:Cell differentiation grade determines distinct FOXA2 contributions to the cis-regulatory networks of pancreatic cancer cells [ATAC-seq]

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Cell differentiation grade determines distinct FOXA2 contributions to the cis-regulatory networks of pancreatic cancer cells [RNA-seq]

Project description:Abnormal differentiation contributes to the spectrum of aberrant properties of tumor cells. Differentiation of both normal and tumor cells is controlled by regulatory networks enforced by transcription factors (TFs) involved in lineage specification. Among them, pioneer factors such as FOXA1/2, are able to bind and make accessible naïve chromatin, thus critically contributing to the establishment of gene regulatory networks. Pancreatic ductal adenocarcinoma (PDAC) is characterized by massive heterogeneity, with the coexistence at all disease stages of well- and poorly-differentiated cells with diverging transcriptional networks. We found that FOXA2, a TF controlling pancreas specification, was expressed in both well- and poorly-differentiated PDAC cells, but it controlled distinct gene expression programs and displayed extensively different genomic distributions because of its partnership with TFs expressed in a differentiation grade-specific manner, such as HNF1 and HOXB8/9 in well- and poorly-differentiated cells, respectively. These data suggest that pioneer TFs such as FOXA2 are versatile transcriptional regulators whose broad contribution to the gene regulatory networks of highly heterogeneous cancers such as PDACs, depends on the differential availability of partner TFs expressed in distinct tumor cells.

2019-09-17 | GSE119931 | GEO

Cell differentiation grade determines distinct FOXA2 contributions to the cis-regulatory networks of pancreatic cancer cells [ChIP-seq]

2019-09-17 | GSE119930 | GEO

Cell differentiation grade determines distinct FOXA2 contributions to the cis-regulatory networks of pancreatic cancer cells [ATAC-seq]

2019-09-17 | GSE128100 | GEO

Cell differentiation grade determines distinct FOXA2 contributions to the cis-regulatory networks of pancreatic cancer cells

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

2019-09-17 | GSE120017 | GEO

Gene expression profile of Huh7 cells upon knock-down of FOXA2 or FOXA2-DS-S

Project description:We used siRNAs to knock-down the gene FOXA2 and the positionally-conserved ncRNA (pcRNA) FOXA2-DS-S is Huh7. We have shown that FOXA2 regulates its own expression by binding its promoter, but it can also affect the expression of the associated pcRNA FOXA2-DS-S. At the same time, we have shown that FOXA2-DS-S is necessary for the expression of the FOXA2 gene. These data suggest that the pcRNA acts locally, in cis, to regulate the expression of FOXA2. With this microarray experiment with aimed to explore further the genome-wide transcriptional effects of FOXA2-DS-S or FOXA2 knock-down.

2018-01-09 | E-MTAB-4517 | biostudies-arrayexpress

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Project description:We performed genome-wide location analysis for Foxa2 to identify its targets in the adult mouse liver. Chromatin isolated from the liver of five adult mice was cross-linked, sheared and immunoprecipitated with a Foxa2-specific antibody. The resulting material, as well as material that was not immunoprecipitated, was uncross-linked, amplified, labeled and hybridized to the Mouse Promoter Chip BCBC-5A. Statistical analysis resulted in a set of 107 genes that are bound by Foxa2. Using computational analyses, we showed that Foxa2 containing cis-regulatory modules are dependent on the strength of the Foxa2 consensus site present.

2008-07-04 | E-MTAB-32 | biostudies-arrayexpress

MicroRNA-590-3p promotes ovarian cancer growth and metastasis via a novel FOXA2-Versican pathway

Project description:Epithelial ovarian cancer (EOC) is the deadliest gynecological cancer. MicroRNAs (miRNAs) are small non-coding RNAs that play important roles in gene regulation and their dysregulation is associated with many diseases. In this study, we determined the expression and function of miR-590-3p in EOC. We found that miR-590-3p levels were higher in high-grade carcinoma when compared to low-grade or tumours with low malignant potential. Interestingly, plasma levels of miR-590-3p were significantly higher in EOC patients than in subjects with benign gynaecological disorders. Transient transfection of miR-590-3p mimics, or stable transfection of mir-590, increased cell growth, migration, and invasion. In vivo studies revealed that mir-590 accelerated tumour growth and metastasis. Using a cDNA microarray, we identified Forkhead box A2 (FOXA2) and Versican (VCAN) as a top downregulated and a top upregulated gene, respectively, by mir-590. We showed that miR-590-3p targeted FOXA2 3’ UTR to suppress its expression. In addition, knockdown of FOXA2 by siRNAs or knockout of FOXA2 by CRISPR/Cas9 enhanced cell proliferation, migration, and invasion. Overexpression of FOXA2 decreased, while knockout of FOXA2 increased, VCAN mRNA and protein levels and ChIP-qPCR revealed that FOXA2 binds to VCAN promoter. Interrogation of the TCGA ovarian cancer database revealed a negative relationship between FOXA2 and VCAN mRNA levels in EOC tumours and that high FOXA2/low VCAN mRNA levels in tumours were positively correlated with patient survival. Finally, overexpression of FOXA2 or silencing of VCAN reversed the effects of mir-590. These findings demonstrate that miR-590-3p promotes EOC development via a novel FOXA2-VCAN pathway.

2018-04-21 | GSE113440 | GEO

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