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HNF1A is a Novel Oncogene and Central Regulator of Pancreatic Cancer Stem Cells [Bru-seq]

ABSTRACT: HNF1A is a Novel Oncogene and Central Regulator of Pancreatic Cancer Stem Cells [Bru-seq]

PROVIDER: PRJNA422593 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6380470.fastq.gz	Fastqsanger.gz
	SRR6380461.fastq.gz	Fastqsanger.gz
	SRR6380471.fastq.gz	Fastqsanger.gz
	SRR6380462.fastq.gz	Fastqsanger.gz
	SRR6380472.fastq.gz	Fastqsanger.gz

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Similar Datasets

HNF1A is a Novel Oncogene and Central Regulator of Pancreatic Cancer Stem Cells [Bru-seq]

Project description:The biological properties of pancreatic cancer stem cells (PCSCs) remain incompletely defined and the central regulators are unknown. By bioinformatic analysis of a PCSC-enriched gene signature, we identified the transcription factor HNF1A as a putative central regulator of PCSC function. Levels of HNF1A and its target genes were found to be elevated in PCSCs and tumorspheres, and depletion of HNF1A resulted in growth inhibition, apoptosis, impaired tumorsphere formation, PCSC depletion, and downregulation of OCT4 expression. Conversely, HNF1A overexpression increased PCSC numbers and tumorsphere formation in pancreatic cancer cells and drove PDA cell growth. Importantly, depletion of HNF1A in primary tumor xenografts impaired tumor growth and depleted PCSCs in vivo. Finally, we established an HNF1A-dependent gene signature in PDA cells that significantly correlated with reduced survivability in patients. These findings identify HNF1A as a central transcriptional regulator of the PCSC state and novel oncogene in pancreatic ductal adenocarcinoma.

2018-09-04 | GSE108149 | GEO

HNF1A is a Novel Oncogene and Central Regulator of Pancreatic Cancer Stem Cells [ChIP-seq]

2018-09-04 | GSE108150 | GEO

HNF1A is a Novel Oncogene and Central Regulator of Pancreatic Cancer Stem Cells

Project description:HNF1A is a Novel Oncogene and Central Regulator of Pancreatic Cancer Stem Cells

| PRJNA422591 | ENA

HNF1A is a Novel Oncogene and Central Regulator of Pancreatic Cancer Stem Cells [ChIP-seq]

Project description:HNF1A is a Novel Oncogene and Central Regulator of Pancreatic Cancer Stem Cells [ChIP-seq]

| PRJNA422594 | ENA

HNF1A is a Novel Oncogene and Central Regulator of Pancreatic Cancer Stem Cells

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

2018-09-04 | GSE108151 | GEO

High depth sequencing of BrU-labeled nascent RNA.

Project description:BrU incorporation into nascent RNA followed by immunoprecipitation with a BrU specific antibody. The nascent RNA was subsequently eluted with BrU competition.

2017-08-22 | GSE92565 | GEO

HNF1A, UTX, H3K27me3 and H3K27ac ChIP-seq in wild-type and UTX- or HNF1A-deficient mouse pancreas

Project description:HNF1A and UTX are putative tumor suppressors in pancreatic cancer. In this study, we have combined mouse genetics, transcriptomics and genome binding studies to link HNF1A and UTX in a molecular mechanism that suppresses pancreatic cancer. In this session, we have profiled UTX, HNF1A, H3K27me3 and H3K27ac in normal and UTX- or HNF1A-deficient mouse pancreas by ChIP-seq experiments. We show that HNF1A recruits UTX to its genomic targets in pancreatic acinar cells, which results in remodeling of the chromatin landscape and activation of a broad transcriptional program of differentiated acinar cells, which in turn indirectly suppresses tumor suppressor pathways.

2019-12-20 | E-MTAB-7944 | biostudies-arrayexpress

UMI-4C in control and HASTER-deficient EndoC-betaH3 cells overexpressing HNF1A

Project description:The HASTER promoter region is a cis-regulatory element that stabilizes the transcription HNF1A. If HASTER is deleted after beta cells have been formed and HNF1A is already stably expressed, HASTER is not required to maintain HNF1A activity, and is only required to provide negative feedback on HNF1A. HNF1A binding to the HASTER promoter mediates the repression of the HNF1A gene itself. To determine whether HNF1A binding to the HASTER promoter remodels 3D chromatin interactions of the HNF1A promoter, we performed UMI-4C experiments in wild type and HASTER-promoter KO EndoC-betaH3 cells with or without doxycycline-induced HNF1A overexpression using the HNF1A promoter as viewpoint.

2022-05-01 | E-MTAB-11473 | biostudies-arrayexpress

High depth sequencing of BrU-labeled nascent RNA in METTL3 depleted cells.

Project description:BrU incorporation into nascent RNA followed by immunoprecipitation with a BrU specific antibody. The nascent RNA was subsequently eluted with BrU competition.

2018-06-19 | GSE114542 | GEO

HNF1A deficiency impairs β-cell fate, granule maturation and function

Project description:Mutations in HNF1A cause Maturity Onset Diabetes of the Young type 3, the second most frequent form of diabetes caused by single gene mutation. We generated human pancreatic stem cell-derived endocrine cells with mutations in HNF1A and show that HNF1A deficiency impairs scβ-cell fate, insulin granule maturation and the secretion of insulin in a glucose responsive manner. Single-cell RNA sequencing reveals that HNF1A orchestrates a network of genes involved in glucose metabolism, zinc transport, calcium ion binding and hormone exocytosis. Furthermore, in both patients and stem cell-derived β-cells, HNF1A deficiency altered the stoichiometry of secreted c-peptide to insulin. Sulfonylurea, used in the treatment of these patients, restored both insulin secretion and stoichiometry. Significantly, uncoupling of c-peptide and insulin secretion as described here questions the common practice in using c-peptide as a proxy to evaluate β-cell function. We also demonstrate that correction of the HNF1A locus restores function, providing a path to cell therapy.

2019-03-16 | GSE128331 | GEO

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