Proto-oncogene proteins c-met, also known as hepatocyte growth factor receptor (HGFR), are cell surface receptors that play a vital role in cell growth, proliferation, migration, and invasion. They are encoded by the MET gene and are involved in various cellular processes, including embryogenesis and tissue regeneration.
Proto-oncogene proteins c-met are activated by binding with their ligand, hepatocyte growth factor (HGF). The binding of HGF to c-Met triggers a cascade of intracellular signaling pathways, including the RAS-ERK and PI3K-AKT pathways, which regulate cell survival, proliferation, and motility.
These proteins are implicated in the development and progression of several cancers, as aberrant activation of c-Met signaling can promote tumor growth, angiogenesis, and metastasis. C-Met overexpression or gene amplification is observed in various malignancies, such as lung, liver, breast, prostate, and colorectal cancers.
Targeting c-Met signaling has emerged as a potential strategy for cancer therapy. Inhibitors of c-Met, such as small molecules or monoclonal antibodies, have been developed to block its activation and disrupt downstream signaling pathways. By inhibiting c-Met, these therapeutic agents aim to inhibit tumor growth, prevent metastasis, and enhance the efficacy of other cancer treatments.
Understanding the functions and dysregulation of proto-oncogene proteins c-met is crucial for developing targeted therapies and improving the prognosis of cancer patients. Ongoing research continues to explore the role of c-Met in cancer biology, paving the way for potential new treatment strategies.
