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KSHV is a principal causative agent of primary effusion lymphoma (PEL). Despite this knowledge about the close relationship between HGF/c-MET network and solid tumors development, the role of HGF/c-MET in KSHV-related malignancies remains mostly unclear. We report that HGF/c-MET pathway is highly ac...
ORGANISM(S): Homo sapiens 
We found that RANKL, expressed by cancer cells or derived from exogenous sources, consistently induced human prostate, breast, kidney, lung and liver cancer cells to colonize or metastasize to bone in an animal model of cancer bone metastasis. RANK-mediated signaling established a premetastatic nich...
ORGANISM(S): Homo sapiens 
HGF has been reported to have both positive and negative effects on carcinogenesis. Here we show that the loss of c-Met signaling in hepatocytes enhanced rather than suppressed the early stages of chemical hepatocarcinogenesis. c-Met conditional knockout mice (c-metfl/fl, AlbCre+/-; MetLivKO) treate...
ORGANISM(S): Mus musculus 
The HGF/c-Met system is an essential inducer of hepatocyte growth and proliferation. Although a fundamental role for the HGF receptor c-Met has been demonstrated in acute liver regeneration its cell specific role in hepatocytes during chronic liver injury and fibrosis progression has not been determ...
ORGANISM(S): Mus musculus 
Systems modelling of the EGFR-PYK2-c-Met interaction network predicted and prioritized synergistic drug combinations for Triple-negative breast cancer
2024-09-02 | BIOMD0000000826 | BioModels
Mass spectrometry was used to determine IQGAP1 is a substrate of MET and c-Src, and is phosphorylated exclusively on Tyr-1510 under conditions with enhanced MET or c-Src cellular activity.
ORGANISM(S): Human 
c-Met induces tumor initiation and stemness in HCC cells through the regulation of CD44s via AKT signaling. Over-expression of CD44s in c-Met and CD44s negative cells induce both a stemness and mesenchymal phenotype independent of c-Met. The down regulation of CD44s or c-Met was compared to Scramble...
ORGANISM(S): Homo sapiens 
Loss of TP53 cooperates with c-MET overexpression to drive hepatocarcinogenesis
Treatment of muscle-invasive bladder cancer remains a major clinical challenge. Aberrant HGF/c-MET upregulation and activation is frequently observed in bladder cancer correlating with cancer progression and invasion. However, the precise mechanisms underlying HGF/c-MET mediated invasion in bladder ...
ORGANISM(S): Homo sapiens (Human) 
2019-08-26 | PXD014736 | Pride
Pro-inflammatory c-Met+ CD4 T cells in multiple sclerosis
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