Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Dissecting the genetic and microenvironmental factors of gastric tumorigenesis in mice

ABSTRACT: Dissecting the genetic and microenvironmental factors of gastric tumorigenesis in mice

PROVIDER: PRJNA780192 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Dissecting the genetic and microenvironmental factors of gastric tumorigenesis in mice

Project description:Gastric cancer (GC) is one of the most frequent and lethal malignancies in the world. However, our understanding of the mechanisms underlying its initiation and progression is limited. Here, we applied genome-edited gastric organoids to establish a series of primary GC models in mice, which elucidated the genetic drivers for sequential transformation from dysplasia to well-differentiated and poorly differentiated GC. Further, we found that the orthotopic GC, but not the subcutaneous GC even with the same genetic drivers, displayed remote metastasis, suggesting critical roles of the microenvironment in GC metastasis. Through single-cell RNA-seq analyses and functional studies, we revealed that the molecular interaction between fibronectin 1 on stomach-specific macrophages and integrin α6β4 on GC cells promoted liver metastasis. Taken together, our studies proposed a new strategy to model GC and dissected the genetic and microenvironmental factors driving the full-range gastric tumorigenesis.

2022-09-05 | GSE188761 | GEO

Dissecting Expression Profiles of Gastric Precancerous Lesions and Early Gastric Cancer to Explore Crucial Molecules in Intestinal-type Gastric Cancer Tumorigenesis

Project description:Dissecting Expression Profiles of Gastric Precancerous Lesions and Early Gastric Cancer to Explore Crucial Molecules in Intestinal-type Gastric Cancer Tumorigenesis

| PRJNA541526 | ENA

Sox2 suppresses gastric tumorigenesis in mice

Project description:Sox2 suppresses gastric tumorigenesis in mice

| PRJNA327569 | ENA

Dissecting Expression Profiles of Gastric Precancerous Lesions and Early Gastric Cancer to Explore Crucial Molecules in Intestinal-type Gastric Cancer Tumorigenesis

Project description:To investigate the changes in molecular expression, biological processes, stemness, immune microenvironment, tumor hallmark activities and co-expression relationships during intestinal-type gastric cancer carcinogenesis and to excavate the prognostic information contained in the carcinogenesis process. RNA expression profiles of ninety-four gastroscope biopsy samples with different stages of precancerous lesions or early gastric cancers and their paired controls were detected by Agilent Microarray.

2020-03-15 | GSE130823 | GEO

Regulation of Hippo/YAP axis by CXCR7 in the tumorigenesis of gastric cancer

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

YAP/TAZ initiates gastric tumorigenesis via upregulation of MYC

Project description:YAP/TAZ initiates gastric tumorigenesis via upregulation of MYC

| PRJNA413934 | ENA

Dissecting the single-cell transcriptome network underlying gastric premalignant lesions and early gastric cancer [10x genomics]

Project description:Dissecting the single-cell transcriptome network underlying gastric premalignant lesions and early gastric cancer [10x genomics]

| PRJNA555477 | ENA

A single-cell culture system for dissecting microenvironmental signaling in development and disease of cartilage tissue

Project description:A single-cell culture system for dissecting microenvironmental signaling in development and disease of cartilage tissue

| PRJNA765048 | ENA

Modeling, dissecting, and subtyping of E-cadherin inactivation-associated diffuse-type gastric adenocarcinoma

Project description:Diffuse-type gastric adenocarcinoma (DGAC) is lethal cancer that is often diagnosed late and resistant to therapeutics. Although hereditary DGAC is mainly characterized by mutations in the CDH1 gene that encodes E-cadherin, the impact of E-cadherin inactivation in DGAC tumorigenesis remains unclear. To address this, we established and characterized a CDH1 loss-associated DGAC model system with a human DGAC single-cell transcriptome. We genetically engineered murine gastric organoids (GOs; Cdh1 KO, KrasG12D, Trp53 KO [EKP]) that recapitulates human DGAC tumorigenesis. Cdh1 depletion is sufficient to 1. Single-cell transcriptomics of human DGAC datasets classified patients into three subtypes (DGAC1, 2, and 3). By transcriptional signature, EKP GOs belong to the DGAC1 subtype displaying CDH1 downregulation and epithelial-mesenchymal transition. Compared to DGAC2 and DGAC3, the DGAC1 subtype was characterized by T cell exhaustion, PILRA-CD99 enrichment, and potential sensitivity to PD1 inhibitors. Additionally, we identified the EZH2-mediated transcriptional circuit as a key regulon specifically activated in EKP and a therapeutic vulnerability. This study unravels the unexpected role of E-cadherin loss in cell lineage plasticity, transcriptional reprogramming, and immune evasion of DGAC and further stratifies DGAC patients by single-cell transcriptomics, providing novel insights into E-cadherin loss-associated DGAC tumorigenesis.

2023-08-07 | GSE226266 | GEO

Single-cell transcriptomic profiling uncovers cellular complexity and microenvironment in gastric tumorigenesis associated with Helicobacter pylori

Project description:Helicobacter pylori (H. pylori) infection is a key initiating factor in the Correa cascade of gastric carcinogenesis, but the comprehensive understanding of the pathogenic mechanisms underlying H. pylori-induced GC remains elusive. Here, we generated a single-cell atlas of gastric tumorigenesis comprising 18 specimens of gastritis, intestinal metaplasia and gastric cancer (GC) with or without H. pylori infection. We identified 48 distinct cell subpopulations including novel rare subtypes, and revealed the influence of H. pylori infection on cellular heterogeneity across neoplastic lesions.

2023-12-11 | GSE249874 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data