作者: Yu-Wen Zhang
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摘要: MET (MNNG HOS transforming gene) is one of the receptor tyrosine kinases whose activities are frequently altered in human cancers, and it a promising therapeutic target. normally activated by its lone ligand, hepatocyte growth factor (HGF), eliciting diverse biological that crucial for development physiology. Alteration HGF-MET axis results inappropriate activation cascade intracellular signaling pathways contributes to hallmark cancer events including deregulated cell proliferation survival, angiogenesis, invasion, metastasis. Aberrant from autocrine or paracrine mechanisms due overexpression HGF and/or ligand-independent mechanism caused activating mutations amplification MET. The literature provides compelling evidence role progression. finding cells often use escape therapies targeting other strengthens argument MET-targeted therapeutics. Diverse strategies have been explored deactivate signaling, compounds biologics pathway clinical development. Despite various trials, we still waiting true therapeutics clinic. This review will explore recent progress hurdles pursuit drugs discuss challenges such