Genome-wide maps of IRF3 and YAP in gastric cancer cells.
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ABSTRACT:
PROVIDER: PRJNA429615 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6463484_1.fastq.gz | Fastqsanger.gz | |||
| SRR6463484_2.fastq.gz | Fastqsanger.gz | |||
| SRR6463485_1.fastq.gz | Fastqsanger.gz | |||
| SRR6463485_2.fastq.gz | Fastqsanger.gz |
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Project description:We performed chromatin immunoprecipitation (ChIP) assays with YAP and IRF3 antibodies in HGC-27 cells. Analysis of the distribution of YAP- or IRF3-binding sites relative to genes annotated in the human genome, revealed that only a minute fraction of peaks mapped close (<1 kb) to transcription start sites (TSSs) whereas most peaks were located farther than 10 kb from the closest TSS. A total of 6,277 peaks were identified by both YAP and IRF3 antibodies.
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Project description:YAP is a transcriptional co-activator of the hippo signaling pathway and is known for its oncogenic and regenerative activity across numerous tissue types. In particular, high YAP levels in patients with gastric cancer (GC) confer a lower survival rate and poor prognosis for these individuals. Therefore, there is a great need to develop targeted therapies against these aggressive tumors. However, the role of YAP and its underlying molecular mechanisms during gastric tumorigenesis are still poorly understood. Using genetic models, we demonstrate the oncogenic function of YAP in CLU+ gastric cells in vivo. YAP over-expression in CLU+ cells induced atrophy, metaplasia and hyperproliferation in the gastric corpus, while its deletion in a Notch activated gastric tumor model rescued metaplasia. Furthermore, we defined the YAP1 targetome in YAP activated gastric tumors, and showed that YAP1 binds to the active chromatin elements of spasmolytic polypeptide-expressing metaplasia (SPEM) related genes and activates their expressions in gastric tumors and ulcers. Together, these results reveal YAP1 as a critical regulator of metaplasia in the gastric corpus, and highlights YAP signaling as a possible therapeutic target to inhibit the progression of gastric tumors.
2023-11-07 | GSE199171 | GEO
Project description:YAP is a transcriptional co-activator of the hippo signaling pathway and is known for its oncogenic and regenerative activity across numerous tissue types. In particular, high YAP levels in patients with gastric cancer (GC) confer a lower survival rate and poor prognosis for these individuals. Therefore, there is a great need to develop targeted therapies against these aggressive tumors. However, the role of YAP and its underlying molecular mechanisms during gastric tumorigenesis are still poorly understood. Using genetic models, we demonstrate the oncogenic function of YAP in CLU+ gastric cells in vivo. YAP over-expression in CLU+ cells induced atrophy, metaplasia and hyperproliferation in the gastric corpus, while its deletion in a Notch activated gastric tumor model rescued metaplasia. Furthermore, we defined the YAP1 targetome in YAP activated gastric tumors, and showed that YAP1 binds to the active chromatin elements of spasmolytic polypeptide-expressing metaplasia (SPEM) related genes and activates their expressions in gastric tumors and ulcers. Together, these results reveal YAP1 as a critical regulator of metaplasia in the gastric corpus, and highlights YAP signaling as a possible therapeutic target to inhibit the progression of gastric tumors.
2023-11-07 | GSE199170 | GEO
Project description:The Hippo pathway is crucial in organ size control and tumorigenesis. The dys-regulation of Hippo/YAP axis is vastly observed in gastric cancer, while the effective therapeutic targets for Hippo/YAP axis are still not clear. It is important and urgent to identify reliable drug targets and the underlying mechanisms, which could inhibit the activity of Hippo/YAP axis and gastric cancer progression. In our current study, we demonstrate the membrane receptor CXCR7 (C-X-C chemokine receptor 7) is an important modulator for Hippo/YAP axis. The activation of CXCR7 could stimulate gastric cancer cell progression through Hippo/YAP axis in vitro and in vivo, while pharmaceutical inhibition of CXCR7 via ACT-1004-1239 could block the tumorigenesis in gastric cancer. Molecular studies reveal that the activation of CXCR7 could dephosphorylate YAP, facilitate YAP nuclear accumulation and transcriptional activation in gastric cancer. CXCR7 functions via G-protein Gαq/11 and Rho GTPase to activate YAP activity. Interestingly, ChIP assay shows that YAP could bind to the promoter region of CXCR7 and facilitate its gene transcription, which indicates CXCR7 is both the upstream signaling and downstream target for Hippo/YAP axis in gastric cancer. In general, we identified a novel positive feedback loop between CXCR7 and Hippo/YAP axis, while blockade of CXCR7 could be a plausible strategy for gastric cancer.
2023-11-15 | GSE233094 | GEO
Project description:Genome-wide binding of IRF3 was analysed in MM1.S cells using ChIP-seq high-throughput approach. MM1.S cells were fixed in 1% formaldehyde (Alfa Aesar) for 15min at room temperature. cells were lysed with hypotonic lysis buffer for 15minutes followed by nuclear lysis buffer for 15min on ice. ChIP for IRF3 performed by a standard ChIP-seq protocol and the genome-wide binding of IRF3 data was analysed which revealed peaks enrichment at cell cycle genes TSS.
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Project description:Genome-wide binding of transcription factor IRF3
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Project description:Purpose: To investigate the signal crosstalk between IRF3 and YAP, RNA-sequencing (RNA-seq) was performed to analyze the genome-wide changes by the knockdown of IRF3 or YAP in HGC-27 cells. Methods: Total RNA was extracted from HGC-27 cell after transfection with negative control siRNA (n.c.), IRF3 siRNA (siIRF3) or YAP siRNA (siYAP). Then total RNA was quality controlled and quantified using an Agilent 2100 Bioanalyzer. After converting to cDNA and building library, high-throughput sequencing was performed using the Illumina HiSeq 2500 platform. Results: Approximately approximately one thousand transcripts showed differential expression between the siIRF3/siYAP and n.c., with a Fold-change>=2 and q-value <= 0.05. Gene ontology (GO) and gene set enrichment analysis (GSEA) showed a significant negative enrichment of YAP target genes identified by three independent studies in IRF3-knockdown condition. Conclusions: We conclude that RNA-seq based transcriptome characterization would provide a framework for understanding the signal crosstalk between IRF3 and YAP.
2018-01-10 | GSE109028 | GEO
Project description:Purpose: To investigate the signal crosstalk between IRF3 and YAP, RNA-sequencing (RNA-seq) was performed to analyze the genome-wide changes by the knockdown of IRF3 or YAP in HGC-27 cells. Methods: Total RNA was extracted from HGC-27 cell after transfection with negative control siRNA (n.c.), IRF3 siRNA (siIRF3) or YAP siRNA (siYAP). Then total RNA was quality controlled and quantified using an Agilent 2100 Bioanalyzer. After converting to cDNA and building library, high-throughput sequencing was performed using the Illumina HiSeq 2500 platform. Results: Approximately one thousand transcripts showed differential expression between the siIRF3/siYAP and n.c., with a Fold-change>=2 and q-value <= 0.05. Gene ontology (GO) and gene set enrichment analysis (GSEA) showed a significant negative enrichment of YAP target genes identified by three independent studies in IRF3-knockdown condition. Conclusions: We conclude that RNA-seq based transcriptome characterization would provide a framework for understanding the signal crosstalk between IRF3 and YAP.
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Project description:Helicobacter pylori(H. pylori), a gastrointestinal pathogen, is known to increase the risk of gastric cancer by activating chronic pro-inflammatory signaling pathways in epithelial cells. Cytotoxin-related protein A (CagA) is known to play an important role in gastric cancer development. CagA has been reported to induce tumors by inducing overexpression of YAP/TAZ, a component of Hippo signaling, and dysregulation of the pathway, thereby promoting cell proliferation and resistance to apoptosis. However, the role of H.pylori-mediated YAP/TAZ has not yet been fully investigated. Our study aimed to investigate the role of YAP/TAZ in H.pylori-mediated Hippo pathway dysregulation in gastric carcinogenesis using H.pylori-infected gastric cancer cell lines, knockout mice, and patient-derived organoids. CagA-mediated YAP overexpression in gastric epithelial cells induced intestinal epithelial metaplasia and induced intracellular rearrangement of the binding protein ZO1, thereby conferring cell motility.
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