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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. 2 — Chemotherapy resistant cancer cells (CRCC) have altered MET signalling, including overexpression of MET, activation sustained by HGF secreted by CAFs (cancer associated fibroblasts), constitutive activation of MET and secretion of HGF which is not normally expressed by epithelial cells, leading to an autocrine activation loop. This diagram illustrates the effect of this altered MET signalling on: (i) the behaviour of CRCCs: reduction of apoptosis, increased proliferation, enhanced DNA repair, upregulation of drug efflux and stimulation of epithelial-mesenchymal transition; (ii) changes in the tumour microenvironment: alteration of the behaviour of endothelial cells and increased intra-tumoural hypoxia, promotion of cancer stem cells (CSCs) survival and proliferation. All these changes contribute to the development of chemotherapy resistance. The intracellular pathways reported or suggested are shown. Blue box/black line: confirmed mechanism. Dotted red box/red line: proposed mechanism. MMPs matrix metallopeptidases, VEGF vascular endothelial growth factor, AIF apoptosis-inducing factor, ER endoplasmic reticulum.