Division of Medical Oncology, Department of Precision Medicine, School of Medicine, University of Campania "Luigi Vanvitelli", Via Pansini n.5, 80131 Naples, Italy.
Int J Mol Sci. 2018 Nov 14;19(11):3595. doi: 10.3390/ijms19113595.
An overactivation of hepatocyte growth factor (HGF)/mesenchymal-epithelial transition factor (MET) axis promotes tumorigenesis and tumor progression in various cancer types. Research data recently evidenced that HGF/MET signaling is also involved also in the immune response, mainly modulating dendritic cells functions. In general, the pathway seems to play an immunosuppressive role, thus hypothesizing that it could constitute a mechanism of primary and acquired resistance to cancer immunotherapy. Recently, some approaches are being developed, including drug design and cell therapy to combine MET and programmed cell death receptor-1 (PD-1)/programmed cell death receptor-ligand 1 (PD-L1) inhibition. This approach could represent a new weapon in cancer therapy in the future.
肝细胞生长因子（HGF）/间质-上皮转化因子（MET）轴的过度激活促进了多种癌症类型的肿瘤发生和肿瘤进展。最近的研究数据表明，HGF/MET 信号通路也参与了免疫反应，主要调节树突状细胞的功能。一般来说，该通路似乎发挥着免疫抑制作用，因此可以假设它可能是癌症免疫治疗原发性和获得性耐药的机制之一。最近，一些方法正在被开发，包括药物设计和细胞治疗，以结合 MET 和程序性细胞死亡受体-1（PD-1）/程序性细胞死亡受体配体 1（PD-L1）抑制。这种方法可能代表未来癌症治疗的一种新武器。
