Abstract
An overactivation of hepatocyte growth factor (HGF)/mesenchymal-epithelial transition factor (MET) axis promotes tumorigenesis and tumor progression in various cancer types. Research data recently evidenced that HGF/MET signaling is also involved also in the immune response, mainly modulating dendritic cells functions. In general, the pathway seems to play an immunosuppressive role, thus hypothesizing that it could constitute a mechanism of primary and acquired resistance to cancer immunotherapy. Recently, some approaches are being developed, including drug design and cell therapy to combine MET and programmed cell death receptor-1 (PD-1)/programmed cell death receptor-ligand 1 (PD-L1) inhibition. This approach could represent a new weapon in cancer therapy in the future.
Highlights
The mesenchymal-epithelial transition factor (MET) gene encodes for a membrane-bound receptor tyrosine kinase (RTK) that is mainly expressed in epithelial cells, the MET receptor
MET RTK is activated by a serum ligand, the hepatocyte growth factor (HGF), which is produced predominately by stromal cells and fibroblasts
Only few datasets are already available on the resistance to the currently used anti-programmed cell death receptor-1 (PD-1)/programmed cell death receptor-ligand 1 (PD-L1) immunotherapy, and further studies are needed to select and identify subpopulations of patients that can derive clinically consistent benefit from these drugs
Summary
The mesenchymal-epithelial transition factor (MET) gene encodes for a membrane-bound receptor tyrosine kinase (RTK) that is mainly expressed in epithelial cells, the MET receptor. METcancers, proteinosteosarcomas, levels increaseand in metaplasia-dysplasia-adenocarcinoma evolution in Taken cancer together, these findings a leading role of MET as the a proto-oncogene in esophageal [10], while higher elucidate levels of HGF are detectable during carcinogenesis of tumorigenesis. EMT, and consequent changes gene and protein phenotype in cancer have which pointed out that oncogene alterations areinvasive involved in In cancer progression, and they are cells, become more malignant and highly the last few decades, researchers potentially targetable, with newalterations molecularly. Resistance is targetable, with newgrowth, molecularly targetedof agents Even if these agents are selective and able to arrest the result of complex interactions among tyrosine (RTKs) and other tumor growth, the majority of patients soonervarious or laterreceptor experience relapse.kinases.
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