The interplay between oxytocin receptor and YAP in regulating gastric cancer progression
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1194148 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31609109.fastq.gz | Fastqsanger.gz | |||
| SRR31609110.fastq.gz | Fastqsanger.gz | |||
| SRR31609111.fastq.gz | Fastqsanger.gz | |||
| SRR31609112.fastq.gz | Fastqsanger.gz | |||
| SRR31609113.fastq.gz | Fastqsanger.gz |
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Project description:Gastric cancer (GC) is one of the most lethal malignancies worldwide, but the effective therapeutic targets for GC is still limited. Accumulated evidence implicates the over-activation of Hippo/YAP axis in GC, while pharmaceutical targeting YAP could be a plausible strategy for GC treatment. Thus, it is of great clinical significance to identify novel hits for Hippo/YAP axis in GC. In our study, we identified oxytocin receptor (OXTR) as an important regulator of Hippo/YAP axis. RNA sequence analysis revealed the OXTR depletion inhibited the expression of Hippo target genes in whole genomic scale.
2024-12-11 | GSE283517 | 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 | 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:Gastric cancer is still one of the most common cancer types and third leading cause of cancer deaths worldwide. Recent studies have showed that the Hippo signaling pathway plays a critical role in progression of gastric cancer. It is of great importance to demonstrate the regulation of Hippo signaling pathway and the degradation of YAP protein in gastric cancer. In this study, we found that OTUB1 is a critical factor to facilitate gastric cancer cell stemness and progression, which deubiquitinated and stabilized YAP protein.
2022-02-24 | GSE197135 | GEO
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.
2024-10-28 | GSE275727 | GEO
Project description:To identify both common and unique transcriptional targets of YAP and TAZ in gastric cancer cells
2020-12-31 | GSE161631 | GEO
Project description:Although aberrant activation of Hippo/YAP has been demonstrated to contribute to the development of gastric cancer, functional studies of this cascade in the context of gastric signet-ring cell carcinoma (GSRC) remain absent. Our previous single-cell sequencing results showed that G protein-coupled estrogen receptor (GPER) is overexpressed in GSRC, and this overexpression is associated with aberrant activation of the Hippo/YAP axis. Identifying effective treatment targets that modulate the Hippo/YAP axis to suppress development of GSRC is of critical importance.GPER was identified as highly overexpressed in GSRC and correlated with worse prognosis. Its activation facilitated tumor proliferation by YAP nuclear translocation and subsequent transcriptional activation. Mechanistically, GPER disrupted LATS1-mediated YAP phosphorylation by competitively binding to ARRB2, thereby enhancing YAP activity. Moreover, YAP bound to the GPER promoter, forming a positive feedback loop that reinforced oncogenic signaling.These findings revealed the key role of the GPER-YAP positive feedback loop in GSRC progression. Targeting this signaling axis, particularly via dual inhibition of GPER and YAP, offered a promising therapeutic strategy for GSRC.
2025-03-28 | GSE283111 | GEO
Project description:The YAP pathway in regulating organ size by integrating external signals to control the expression of genes involved in cell proliferation. YAP is known to be involved in tumorigenesis in several tissues, yet its role in cholangiocarcinoma is not established We used microarrays to assess the role of YAP pathway in cholangiocarcinoma either by overexpressing a constitutively active YAP1 mutant, or by downregulating YAP1 expression using shRNA HuCCT1 cells where transfected with either an empty vector or a vector overexpressing the constitutively active YAP1 S127A; cells were harvested, RNA was collected and analyzed using microarray
2015-10-27 | E-GEOD-61764 | biostudies-arrayexpress
Project description:The YAP pathway in regulating organ size by integrating external signals to control the expression of genes involved in cell proliferation. YAP is known to be involved in tumorigenesis in several tissues, yet its role in cholangiocarcinoma is not established We used microarrays to assess the role of YAP pathway in cholangiocarcinoma either by overexpressing a constitutively active YAP1 mutant, or by downregulating YAP1 expression using shRNA HuCCT1 cells where transfected with either a control scrambled shRNA or a shRNA targeting YAP1; cells were harvested, RNA was collected and analyzed using microarray
2015-10-27 | E-GEOD-61765 | biostudies-arrayexpress