Hnf4a regulated transcriptome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA574921 | ENA |
REPOSITORIES: ENA
Dataset's files
| 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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Project description:Hnf4a regulated transcriptome in murine PDAC autochthonous tumors [FFPE tumors]
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Project description:Long noncoding RNAs (lncRNAs), one type of endogenous RNA longer than 200 nucleotides, play emerging roles in tumorigenesis and aggressiveness. However, the functions and underlying mechanisms of lncRNAs in regulating neuroblastoma progression still remain elusive. We identify HNF4A antisense RNA 1 (HNF4A-AS1), a lncRNA derived from upstream region of hepatocyte nuclear factor 4 alpha (HNF4A), as a novel driver of neuroblastoma progression. To investigate the mechanisms underlying the oncogenic functions of HNF4A-AS1, we employed the Illumina HiSeq X Ten as a discovery platform to analyze the transcriptome profiling changes of human neuroblastoma SH-SY5Y cells in response to stable over-expression of HNF4A-AS1. The results showed that stable over-expression of HNF4A-AS1 led to altered expression of 4296 human mRNAs, including 2169 up-regulated genes and 2127 down-regulated genes. Furthermore, we validated the RNA-seq results by real-time RT-PCR with high identity. Overall, our results provided fundamental information about the transcriptomic changes in response to HNF4A-AS1 over-expression in human tumor cells, and these findings will help us understand the pathogenesis of tumor progression.
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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.
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Project description:Hnf4a regulated transcriptome in 2D cell lines derived from murine pancreatic tumors [2D cell lines]
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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.
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Project description:Specific regulation of target genes by transforming growth factor-β (TGF-β) in a given cellular context is determined in part by transcription factors and cofactors that interact with the Smad complex. In the present study, we determined Smad2 and Smad3 (Smad2/3) binding regions in the promoters of known genes in HepG2 hepatoblastoma cells, and compared them to those in HaCaT epidermal keratinocytes to elucidate the mechanisms of cell type- and context-dependent regulation of transcription induced by TGF-β. Our results show that 81% of the Smad2/3 binding regions in HepG2 cells were not shared with those found in HaCaT cells. Hepatocyte nuclear factor 4α (HNF4α) is expressed in HepG2 cells, but not in HaCaT cells, and the HNF4α binding motif was identified as an enriched motif in the HepG2-specific Smad2/3 binding regions. ChIP-sequencing analysis of HNF4A binding regions under TGF-β stimulation revealed that 32.5% of the Smad2/3 binding regions overlapped HNF4A bindings. MIXL1 was identified as a new combinatorial target of HNF4A and Smad2/3, and both the HNF4A protein and its binding motif were required for the induction of MIXL1 by TGF-β in HepG2 cells. These findings generalize the importance of binding of HNF4A on Smad2/3 binding genomic regions for HepG2-specific regulation of transcription by TGF-β, and suggest that certain transcription factors expressed in a cell-type-specific manner play important roles in the transcription regulated by the TGF-β-Smad signaling pathway. HepG2 cells were treated with TGF-beta for 1.5 h or left untreated. anti-HNF4A ChIP-seq was performed. One lane was used for each sample.
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