1. Figure 3 The contribution of the tumour microenvironment
to the activation of the epithelial-to mesenchymal transition (EMT) programme
Figure 3 | The contribution of the tumour microenvironment to the activation of the epithelial-to-mesenchymal transition (EMT) programme. a | Carcinoma-associated fibroblasts (CAFs) are frequently observed at the invasive front of tumours, and probably make an important contribution to the induction of EMT in nearby carcinoma cells by secreting various cytokines and enzymes. b | The tumour microenvironment is often characterized by chronic inflammation; both soluble and cellular mediators of tumour-associated inflammation can contribute to the induction of an EMT programme in carcinoma cells. c | Hypoxia is another common characteristic of the tumour microenvironment. HIF-1, the central mediator of the responses to tumour-associated hypoxia, has been demonstrated to trigger an EMT process, involving the prototypic transcription factors ZEB1/2, TCF-3, and TWIST1, in carcinoma cells. CCL18, C–C-motif chemokine 18; HGF, hepatocyte growth factor; HIF-1, hypoxia-inducible factor 1; MMP, matrix metalloproteinase; TGFβ, transforming growth factor β; TNFα, tumour necrosis factor α; uPA, urokinase plasminogen activator.
Shibue, T. & Weinberg, R. A. (2017) EMT, CSCs, and drug resistance: the mechanistic link and clinical implications
Nat. Rev. Clin. Oncol. doi: /nrclinonc