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YAP-activated metaplasia underlies gastric adenocarcinoma and corpus regenerative mechanisms [RNA-Seq]

ABSTRACT: YAP-activated metaplasia underlies gastric adenocarcinoma and corpus regenerative mechanisms [RNA-Seq]

PROVIDER: PRJNA818690 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18434337_1.fastq.gz	Fastqsanger.gz
	SRR18434337_2.fastq.gz	Fastqsanger.gz
	SRR18434338_1.fastq.gz	Fastqsanger.gz
	SRR18434338_2.fastq.gz	Fastqsanger.gz
	SRR18434339_1.fastq.gz	Fastqsanger.gz

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YAP-activated metaplasia underlies gastric adenocarcinoma and corpus regenerative mechanisms

Project description:YAP-activated metaplasia underlies gastric adenocarcinoma and corpus regenerative mechanisms

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YAP-activated metaplasia underlies gastric adenocarcinoma and corpus regenerative mechanisms [RNA-Seq]

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.

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YAP-activated metaplasia underlies gastric adenocarcinoma and corpus regenerative mechanisms [ChIP-Seq]

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YAP-activated metaplasia underlies gastric adenocarcinoma and corpus regenerative mechanisms [ChIP-Seq]

Project description:YAP-activated metaplasia underlies gastric adenocarcinoma and corpus regenerative mechanisms [ChIP-Seq]

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Project description:This SuperSeries is composed of the SubSeries listed below.

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Pharmacological YAP activation promotes regenerative repair of cutaneous wounds.

Project description:Chronic cutaneous wounds remain a persistent unmet medical need that decrease expectancy and quality of life. Here, we report that topical application of PY-60, a small molecule activator of the transcriptional coactivator YAP, promotes regenerative repair of cutaneous wounds in pig and human models. Pharmacological YAP activation enacts a reversible pro-proliferative transcriptional program in keratinocytes and dermal cells that results in accelerated re-epithelization and regranulation of the wound bed. These results demonstrate that transient topical administration of a YAP activating agent may represent a generalizable therapeutic approach to treating chronic wounds.

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Transcriptional analysis reveals the molecular details of atrophic gastritis in Helicobacter pylori infected corpus mucosa

Project description:The majority of gastric cancer cases are believed to be caused by chronic infection with the bacterium Helicobacter pylori, and atrophic corpus gastritis is a predisposing condition to gastric cancer development. We aimed to increase understanding of the molecular details of atrophy by performing a global transcriptome analysis of stomach tissue. Biopsies from patients with different stages of H. pylori infection were taken from both the antrum and corpus mucosa and analyzed on microarrays. The stages included patients without current H. pylori infection, H. pylori-infected without corpus atrophy and patients with current or past H. pylori-infection with corpus-predominant atrophic gastritis.Using clustering and integrated analysis, we found firm evidence for antralization of the corpus mucosa of atrophy patients. This antralization harbored gain of gastrin expression, as well as loss of expression of corpus-related genes, such as genes associated with acid production, energy metabolism and blood clotting. The analyses provided detailed molecular evidence for simultaneous intestinal metaplasia (IM) and spasmolytic polypeptide expressing metaplasia (SPEM) in atrophic corpus tissue. Finally, acidic mammalian chitinase, a chitin-degrading enzyme produced by chief cells, was shown to be strongly down-regulated in corpus atrophy.Transcriptome analysis revealed several gene groups which are related to development of corpus atrophy, some of which were increased also in H. pylori-infected non-atrophic patients. Furthermore, loss of acidic chitinase expression is a promising marker for corpus atrophy. Biopsies from well classified patients with different stages of H. pylori infection were taken from both the antrum and corpus mucosa. These stages included H. pylori un-infected, H. pylori-infected without corpus atrophy and H. pylori-infected with corpus-predominant atrophic gastritis.

2014-02-04 | E-GEOD-27411 | biostudies-arrayexpress

Pharmacological YAP activation promotes regenerative repair of cutaneous wounds.

Project description:Pharmacological YAP activation promotes regenerative repair of cutaneous wounds.

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Transcriptional analysis reveals the molecular details of atrophic gastritis in Helicobacter pylori infected corpus mucosa

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Endogenous glucocorticoids suppress spontaneous gastric inflammation and spasmolytic polypeptide expressing metaplasia

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