以c-Met为肿瘤治疗靶点的受体酪氨酸激酶抑制剂的研究进展

受体酪氨酸激酶c-Met在细胞的增殖、代谢以及肿瘤的产生、转移、血管生成中扮演着重要角色，c-Met成为抗肿瘤治疗的重要靶点。HGF/c-Met信号通路与VEGFR等其他通路的相互作用(cross-talk)影响了抗肿瘤药物的作用效果，产生耐药性，因此，多激酶靶点联合用药成为新的抗肿瘤治疗手段。本文介绍了c-Met信号通路与多种膜受体间的相互作用以及由这种相互作用引起的对激酶抑制剂的耐药性，并综述了单靶点和多靶点的小分子c-Met抑制剂的研究进展。
c-Met receptor tyrosine kinase plays an important role in signaling pathways including cell proliferation, metabolism as well as tumorigenic growth, migration and angiogenesis. c-Met has emerged as an attractive target for cancer therapy. Moreover, the interactive cross-talk between c-Met signaling and several other signaling pathways underlies a key effect for resistance of anti-cancer drugs. Thus, multi-target inhibitors become a new approach to cancer therapy. This paper introduces the c-Met signaling pathway and the resistance of kinase inhibitors caused by the cross-talk between c-Met and other membrane receptors and then will reviews the progress of single-target and multi-target c-Met inhibitors