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YAP orchestrates heterotypic endothelial cell communication via HGF/c-MET signaling in liver tumorigenesis

ABSTRACT: YAP orchestrates heterotypic endothelial cell communication via HGF/c-MET signaling in liver tumorigenesis

PROVIDER: PRJNA526207 | ENA |

REPOSITORIES: ENA

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YAP orchestrates heterotypic endothelial cell communication via HGF/c-MET signaling in liver tumorigenesis

Project description:YAP orchestrates heterotypic endothelial cell communication via HGF/c-MET signaling in liver tumorigenesis

| PRJNA526203 | ENA

YAP orchestrates heterotypic endothelial cell communication via HGF/c-MET signaling in liver tumorigenesis

Project description:YAP orchestrates heterotypic endothelial cell communication via HGF/c-MET signaling in liver tumorigenesis

| PRJNA526205 | ENA

YAP orchestrates heterotypic endothelial cell communication via HGF/c-MET signaling in liver tumorigenesis

Project description:Disturbance of heterologous cell communication is associated with a structural reorganization of the vascular niche, a process called capillarization, which is already initiated in early stages of liver tumor development. In this study, the molecular characterization of endothelial cell (EC) subpopulations from healthy livers and yes-associated protein (Yap)-induced liver tumors revealed a dynamic crosstalk between liver sinusoidal endothelial cells (LSECs) and capillary endothelial cells (CECs). Initial paracrine stimuli from parenchymal cells include the Yap/Tead4 target gene osteopontin (Opn), which promotes CECs expansion through the induction of c-Met and sensitization towards LSEC-derived hepatocyte growth factor (Hgf). In addition, Yap/Tead4-induced C-C motif chemokine ligand 2 (Ccl2) recruits bone-marrow-derived macrophages (BMDMs) with an unpolarized phenotype (M0) to the perivascular space of expanding CECs.

2020-09-15 | GSE128046 | GEO

YAP orchestrates heterotypic endothelial cell communication via HGF/c-MET signaling in liver tumorigenesis

2020-09-15 | GSE128044 | GEO

YAP orchestrates heterotypic endothelial cell communication via HGF/c-MET signaling in liver tumorigenesis

2020-09-15 | GSE128042 | GEO

An endothelial subtype-specific communication network orchestrates capillarization in liver tumorigenesis via the Hgf/c-Met pathway

Project description:An endothelial subtype-specific communication network orchestrates capillarization in liver tumorigenesis via the Hgf/c-Met pathway

| PRJNA526201 | ENA

The Influence of Met Receptor Level on HGF-Induced Glycolytic Reprogramming in Head and Neck Squamous Cell Carcinoma

Project description:Head and neck squamous cell carcinomas (HNSCC) are known to overexpress a variety of receptor tyrosine kinases, such as the HGF receptor Met. Like other malignancies, there is a mutual interaction between the tumor cells and surrounding tissues and cells. We hypothesized that activation of HGF/Met signaling in HNSCC might influence glucose metabolism and therefore substantially changes the tumor microenvironment. To determine the effect of HGF, we used three established HNSCC cell lines and flow cytometry, western blot and RNA sequencing. Dynamic changes in glucose metabolism were measured real-time by an Extracellular flux analyzer. As expected, the cell lines exhibited different levels of Met and responded differently to HGF stimulation. As confirmed by RNA sequencing, the level of Met expression is associated with the number of upregulated HGF-dependent genes. Overall, Met stimulation by HGF leads to increased glycolysis, presumably mediated by higher expression of three key enzymes of glycolysis. These effects appear to be stronger in Methigh expressing HNSCC cells. Collectively our data supports the hypothesized role of HGF/Met signaling in metabolic reprogramming of HNSCC.

2020-01-17 | GSE135552 | GEO

Functional Comparison of the HGF/Met and MSP/Ron Systems in a Pancreatic Cancer Model

Project description:Pancreatic cancer is an aggressive disease with a poor prognosis for which current standard chemotherapeutic treatment options offer little survival benefit. In recent years, receptor tyrosine kinases (RTK)s have garnered interest as therapeutic targets to augment or replace standard chemotherapeutic therapies because of their high expression levels in various cancers and their ability to promote cell growth, migration, and survival. Met and Ron, which are homologous RTKs activated by the ligands hepatocyte growth factor (HGF) and macrophage stimulating protein (MSP), respectively, are over-activated in many of the least treatable cancers. In pancreatic adenocarcinoma, Met expression is linked to poor patient survival and Ron expression is generally higher in tumor samples relative to normal tissue, although its prognostic significance in pancreatic cancer remains unclear. Despite the structural homology between Met and Ron, studies that have directly compared the functional outcomes of these systems in any context are limited. To address this, we sought to determine if the HGF/Met and MSP/Ron systems produce overlapping or divergent contributions towards a malignant phenotype by performing a characterization of MSP and HGF driven signaling, behavioral, and transcriptomic responses in pancreatic cancer cells in vitro. We found HGF and MSP both encouraged cell migration and activated the MAPK/Erk pathway both at the transcript and protein level. HGF uniquely increased proliferation in addition to regulating a wider variety of transcripts compared to MSP. Although HGF and MSP produced a differing breadth of responses, overlapping pro-cancer signaling, behavioral, and transcriptional effects suggest dual inhibition of the MSP/Ron and HGF/Met systems in pancreatic cancer may provide a more complete anti-cancer effect compared to individually targeting either system.

2019-06-14 | GSE129075 | GEO

Trancriptome profiling of genome-edited 16HBE cells on the receptor tyrosine kinase MET in response to HGF

Project description:Effect of MET exon 14 skipping on gene expression stimulated or not by its ligand Hepatocyte Growth Factor (HGF) in pulmonary epithelial 16HBE cell line which undergone genome-editing by CRISPR-Cas9 technology.

2023-11-16 | GSE184514 | GEO

Expression data of RPTEC cells treated with/without HGF, aMD5-PEG11 and aMD5-BMH

Project description:We synthesized HGF mimic Met-agonist, which is a kind of Met high-affinity dimeric peptide that can activate the Met through dimerization of Met, and induce cell growth, migration, and branching morphogenesis in a similar manner to HGF. Here we detected the gene expression profile induced by HGF and artificial Met-agonist (aMD5-PEG11 and aMD5-BMH). HGF and aMD5-PEG11 show similar induction of gene expression pattern, including multicellular organismal development, multicellular organismal process and anatomical structure development.

2018-11-30 | GSE111542 | GEO

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