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. 2021 Feb 1;40(11):1927–1941. doi: 10.1038/s41388-020-01577-5

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — HGF binding to MET triggers MET dimerisation and phosphorylation. Several signalling pathways are then activated, leading to the activation of signals including ERK1/2, STAT3, PI3K and Rac1. Cells respond in increasing their proliferation, migration and/or survival. In parallel, HGF binding to MET triggers its internalisation. MET is still bound to HGF and continues to signal on endosomes. MET internalisation has been shown to be required to sustain its signalling. MET slowly gets degraded, leading to signal termination but oncogenic MET mutants are protected against degradation and trigger persistent endosomal signalling, contributing to their oncogenicity.