C-MET
C-MET (also known as MET proto-oncogene, receptor tyrosine kinase) is a protein that in humans is encoded by the MET gene. C-MET is a member of the receptor tyrosine kinase family and is involved in various cellular processes, including cell growth, motility, and differentiation.
Function[edit | edit source]
C-MET is a receptor for hepatocyte growth factor (HGF), also known as scatter factor. Upon binding to HGF, c-MET undergoes autophosphorylation on its intracellular domain, which activates its kinase activity. This activation triggers a cascade of downstream signaling pathways, including the PI3K/AKT pathway, RAS/MAPK pathway, and STAT3 pathway, which are involved in promoting cell survival, proliferation, and migration.
Clinical significance[edit | edit source]
C-MET has been implicated in the development and progression of various types of cancer, including lung cancer, gastric cancer, and renal cell carcinoma. Overexpression or mutation of the MET gene can lead to oncogenesis by promoting tumor growth, angiogenesis, and metastasis.
Inhibitors targeting c-MET are being developed as potential cancer therapies. These include small molecule inhibitors and monoclonal antibodies that block the interaction between c-MET and HGF or inhibit its kinase activity.
Interactions[edit | edit source]
C-MET interacts with several proteins and signaling molecules, including GRB2, GAB1, and PIK3R1, which are involved in mediating its downstream effects. These interactions are crucial for the activation of signaling pathways that regulate cellular responses to HGF.
See also[edit | edit source]
References[edit | edit source]
External links[edit | edit source]
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Contributors: Prab R. Tumpati, MD