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肝细胞生长因子受体(mesenchymal-epithelial transition factor,MET)通路在肿瘤发生过程中具有重要作用,包括促进细胞增殖、抑制细胞凋亡、促进肿瘤血管生成、促进肿瘤细胞迁移及侵袭、转移等多个过程,涉及质膜、胞内共作用因子及下游效应蛋白的协同作用。体内、外实验证实,MET与表皮生长因子受体(epithelial growth factor receptor,EGFR)之间存在复杂的交互作用,两者共同参与细胞增殖、细胞运动及下游信号通路活化等多种细胞生物学事件,其中一些与肿瘤发生、进展密切相关。MET有可能通过“置换”EGFR活性而参与EGFR抑制剂的耐药发生。文中综述了肝细胞生长因子(hepatocyte growth factor,HGF)-MET和EGFR通路在肿瘤发生、发展过程中的重要作用,讨论了两者交互作用引起EGFR抑制剂耐药的可能机制,在此基础上提出联合使用EGFR和MET靶向抑制剂在克服EGFR抑制剂获得性耐药方面的应用前景。
The mesenchymal-epithelial transition factor (MET) pathway plays an important role in tumorigenesis, including promoting cell proliferation, inhibiting apoptosis, promoting tumor angiogenesis, and promoting tumor cell migration, invasion and metastasis A process involves the synergism of the plasma membrane, intracellular co-factor and downstream effector proteins. Both in vivo and in vitro experiments show that there is a complex interaction between MET and epithelial growth factor receptor (EGFR), both of which are involved in various cellular biological events such as cell proliferation, cell motility and downstream signaling pathway activation , Some of which are closely related to tumorigenesis and progression. It is possible that MET participates in the development of EGFR inhibitor resistance through “replacement ” EGFR activity. In this review, the important role of hepatocyte growth factor (HGF) -MET and EGFR pathways in tumorigenesis and progression was reviewed. The possible mechanism of the interaction between them was also discussed. Based on this, Proposed the combined use of EGFR and MET targeted inhibitors in the acquisition of EGFR inhibitors acquired resistance prospects.