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The effect of K458R mutation of HNF4A on HCC

ABSTRACT: The effect of K458R mutation of HNF4A on HCC

PROVIDER: PRJNA935272 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23462690.fastq.gz	Fastqsanger.gz
	SRR23462691.fastq.gz	Fastqsanger.gz
	SRR23462692.fastq.gz	Fastqsanger.gz
	SRR23462693.fastq.gz	Fastqsanger.gz
	SRR23462694.fastq.gz	Fastqsanger.gz

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The effect of K458R mutation of HNF4A on HCC

Project description:To investigate the inhibitory effect of K458R mutation of HNF4A on HCC, we established Huh-7 xenografts treated with Ad-GFP, Ad-HNF4A or Ad-K458R. We then performed gene expression profiling analysis using data obtained from RNA-seq of three groups of Huh-7 xenografts treated with adenovirus.

2023-02-20 | GSE225329 | GEO

HNF4A functions as an HCC oncogene or tumor suppressor depending upon the AMPK pathway activity status

Project description:Background & Aims: Hepatocyte nuclear factor 4A (HNF4A) is a master transcription factor (TF) in hepatocytes that regulates metabolism and differentiation. The mechanism of HNF4A in cancer progression remains unclear due to conflicting results observed in numerous studies. We aimed to address the roles of HNF4A in hepatocellular carcinoma (HCC). Methods: We established the HNF4A overexpression and knocking-down stable cells in HCCLM3 and Huh7, and compared the effects of HNF4A on HCC cells in different glucose supply conditions in vitro and in vivo. Pathway inhibitors treatment and phosphatase activity comparisons were performed for signaling pathway analysis. Gene levels in HCC tissues and the clinical information were collected from TCGA for survival analysis. Multiomics approaches including proteomics, TFRE and ChIP-seq were applied to identify HNF4A target genes. Rescue experiments were performed to verify the functions of the potential target genes. Results: We found HNF4A exhibited tumor-suppressive effects on proliferation and migration of HCC cells in glucose-sufficient conditions but tumor-promotive effects in glucose-insufficient conditions. This diverse functionality of HNF4A was dependent upon the AMPK pathway activity. Similarly, the prognosis predicted by HNF4A was also correlated with AMPKa expression level in HCC patients. The potential HNF4A target genes, including NEDD4 and RPS6KA2, are involved in the diverse functionality of HNF4A in response to AMPK activity status. Conclusions: The glucose supply status could be the potential decisive factor to determine functions of HNF4A on HCC cells. The switch of HNF4A between oncogene and tumor suppressor was determined by AMPK activation status, which was correlated with glucose levels.

2019-08-01 | GSE101553 | GEO

Effect of loss of HNF4A in liver and effect of ectopic expression of HNF4A in mouse fibroblast cells

Project description:To understand how HNF4A loss affects gene expression in mouse liver. We used control and HNF4A KO mouse livers for RNA sequencing. In addition, we also examined the effect of HNF4A gain in mouse fibroblast cells by ectropically expressing HNF4A in NIH3T3 cell to identify genes that are regulated by HNF4A.

2024-01-15 | GSE210842 | 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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HNF4A

Project description:HNF4A

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Effect of loss of HNF4A in liver and effect of ectopic expression of HNF4A in mouse fibroblast cells

Project description:Effect of loss of HNF4A in liver and effect of ectopic expression of HNF4A in mouse fibroblast cells

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Project description:A specific missense mutation in the DNA binding domain of HNF4A, R85W, causes Fanconi renotubular syndrome (FRTS). To confirm results found in Drosophila, a direct reprogramming approach was applied. Induced renal epithelial tubular cells (iRECs) were generated using transcription factors Hnf1b, Pax8 and either HNF4A WT or HNF4A R85W. RNA Seq analysis of reprogrammed cells shows mitochondrial dysfunction caused by the R85W mutation.

2019-12-16 | GSE139674 | GEO

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