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Hnf4a regulated transcriptome in organoid cultures derived from murine pancreas where HNnf4a is deleted after tumor initiation. [organoid]

ABSTRACT: Hnf4a regulated transcriptome in organoid cultures derived from murine pancreas where HNnf4a is deleted after tumor initiation. [organoid]

PROVIDER: PRJNA574922 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10202304_1.fastq.gz	Fastqsanger.gz
	SRR10202304_2.fastq.gz	Fastqsanger.gz
	SRR10202305_1.fastq.gz	Fastqsanger.gz
	SRR10202305_2.fastq.gz	Fastqsanger.gz
	SRR10202306_1.fastq.gz	Fastqsanger.gz

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Hnf4a regulated transcriptome in organoid cultures derived from murine pancreas where HNnf4a is deleted after tumor initiation. [organoid]

Project description:Pancreatic ductal adenocarcinoma is an aggressive disease with a dismal five-year survival of 5%. Gene expression profiling has been instrumental for subtype classification in cancer, highlighting fundamental differences in tumors at the molecular level. Over the last years, multiple genomics studies have led to the classification of PDAC into two major subtypes: classical and basal-type. The classical subtype expresses higher levels of endodermal lineage specifiers, including HNF4A, GATA6, FOXA2, FOXA3 than the basal-type. The basal-type confers a worse prognosis, raising the possibility that loss of these lineage specifiers might enhance the malignant potential of PDAC. We found that the lineage specifier HNF4a plays a key role in maintaining a transcriptional network that characterizes the classical subtype, restraining growth in different PDAC models. Additionally, we demonstrated that HNF4a controls PDAC cell identity and proliferation, and represses the expression of SIX family members, two mesodermal lineage specifiers highly expressed in basal-type.

2021-01-14 | GSE138142 | GEO

Effects of overexpressing HNF4A on 3D cultured mouse and human colon organoid

Project description:To test the hypothesis that HNF4A should engage small intestine enhancers in colon and activate transcription, we over-expressed HNF4A in 2 independent mouse colonic orgnaoid lines and 5 independent human colonic organoid lines and performed RNA-seq studies. Both RNA-seq data revealed that small intestine functional pathways including fat, protein and carbohydrate digestion and absorption were activated after HNF4A OE. This gain-of-function study of HNF4A in mouse and human colon organoid supports HNF4A as a central mediator of small intestine gene activation in colonic plasticity, conserved across species.

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Project description:<p>We generated a collection of patient-derived pancreatic normal and cancer organoids. We performed whole genome sequencing, targeted exome sequencing, and RNA sequencing on organoids as well as matched tumor and normal tissue if available. This dataset is a valuable resource for pancreas cancer researchers, and those looking to compare primary tissue to organoid culture. In our linked publication, we show that pancreatic cancer organoids recapitulate the mutational spectrum of pancreatic cancer. Furthermore, RNA sequencing of organoids demonstrates the presence of both transcriptional subtypes of pancreas cancer.</p>

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Cleavage under targets and release using nuclease (CUT&RUN) sequencing for HNF4A in human adult kidney and kidney organoid-derived proximal tubular cells

Project description:We performed CUT&RUN sequencing to characterize HNF4A binding sites in human adult kidney and kidney organoid-derived proximal tubular cells.

2023-10-23 | GSE226440 | GEO

Loss-of-function due to MODY1/HNF4A mutation abrogates liver and pancreas differentiation from MODY1-hiPSCs

Project description:Purpose: To investigate the impact of MODY1/HNF4A mutation on foregut development using differentiated control and MODY1-hiPSCs Methods: RNA-Seq was performed on foregut/hepato-pancreatic progenitors obtained on day 14 of the directed differentiation of hiPSCs from MODY1 patients (3 clones from iN904-1, 1 clone from iN904-2) and family controls (3 clones from iN904-7, 2 clones from iN904-13). Differential expression analysis, KEGG pathway and gene ontology analyses were carried out. qRT-PCR validation was also performed using SYBR Green assays. Results: RNA-Seq and transcriptional analyses revealed that numerous foregut liver- and pancreas-related genes, including HNF4A, were downregulated in MODY1-hiPSC-derived hepato-pancreatic progenitors with a fold change ≥1.5 and p value <0.05, whereas hindgut HOX genes were upregulated. Altered expression of a number of genes were further confirmed with qRT-PCR. Conclusions: The HNF4A loss-of-function mutation (p.Ile271fs) resulted in significantly reduced HNF4A expression or HNF4A haploinsufficiency, affecting the proper development of the foregut and its derivatives. This deficiency is propagated to both hepatic and pancreatic cell fates, and may account for β cell developmental defects and the progressive deterioration of β cell function in MODY1.

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Effects of overexpressing HNF4A on 3D cultured mouse and human colon organoid

Project description:Effects of overexpressing HNF4A on 3D cultured mouse and human colon organoid

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Hormone responsive organoid cultures of human endometrium

Project description:Endometrial gland cultures were established from human non-pregnant endometrium and decidua. We analysed the global gene expression profile of the human endometrial gland organoid cultures to assess the similarity of their molecular signature to the tissue of origin. Organoid cultures established from decidua were also included in the analysis to assess their similarity to endometrial dervied cultures.

2017-04-11 | GSE83281 | GEO

TAF4 promotes pre-initiation complex formation and HNF4A occupancy of regulatory elements required to activation post-natal gene expression programme in hepatocytes (ChIP-seq)

Project description:The nuclear receptor HNF4A regulates embryonic and post-natal hepatocyte gene expression. Using hepatocyte-specific inactivation in mice, we show that the TAF4 subunit of TFIID acts as a cofactor for HNF4A in vivo and that HNF4A interacts directly with the TAF4-TAF12 heterodimer in vitro. In vivo, TAF4 is required to maintain HNF4A-directed embryonic gene expression at post-natal stages and for HNF4A-directed activation of post-natal gene expression. TAF4 promotes HNF4A occupancy of functional cis-regulatory elements located adjacent to the transcription start sites of post-natal expressed genes and for pre-initiation complex formation required for their expression. Promoter-proximal HNF4A-TFIID interactions are therefore required for pre-initiation complex formation and stable HNF4A occupancy of regulatory elements as two concomitant mutually dependent processes. Examination of PIC, H3k4me3, Ctcf and Hnf4a occupancy in wild-type and Taf4-/- livers by deep sequencing

2014-09-25 | E-GEOD-57807 | biostudies-arrayexpress

TAF4 promotes pre-initiation complex formation and HNF4A occupancy of regulatory elements required to activation post-natal gene expression programme in hepatocytes (RNA-seq)

Project description:The nuclear receptor HNF4A regulates embryonic and post-natal hepatocyte gene expression. Using hepatocyte-specific inactivation in mice, we show that the TAF4 subunit of TFIID acts as a cofactor for HNF4A in vivo and that HNF4A interacts directly with the TAF4-TAF12 heterodimer in vitro. In vivo, TAF4 is required to maintain HNF4A-directed embryonic gene expression at post-natal stages and for HNF4A-directed activation of post-natal gene expression. TAF4 promotes HNF4A occupancy of functional cis-regulatory elements located adjacent to the transcription start sites of post-natal expressed genes and for pre-initiation complex formation required for their expression. Promoter-proximal HNF4A-TFIID interactions are therefore required for pre-initiation complex formation and stable HNF4A occupancy of regulatory elements as two concomitant mutually dependent processes. RNA profiles in wild-type and Taf4-/- livers by deep sequencing

2014-09-25 | E-GEOD-57712 | biostudies-arrayexpress

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