Figure 4 The mechanistic link between the epithelial-to-mesenchymal

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Figure 4 The mechanistic link between the epithelial-to-mesenchymal transition (EMT) programme and cancer stem cell (CSC) status Figure 4 | The mechanistic link between the epithelial-to-mesenchymal transition (EMT) programme and cancer stem cell (CSC) status. a | The EMT programme enables carcinoma cells to interact productively with the surrounding extracellular matrix (ECM) proteins. Such changes in cell interactions with the ECM, in turn, reinforce the tumour- initiating ability of cancer cells with an active EMT programme. In particular, EMT enables the efficient development by carcinoma cells of integrin-containing mature adhesion plaques, and these plaques, once formed, trigger signalling pathways critical to the proliferation of cancer cells, such as those involving focal adhesion kinase (FAK) and extracellular signal-related kinase (ERK). b | The activation of the EMT programme results in the establishment of several autocrine signalling loops, including the transforming growth factor β (TGFβ) and canonical and/or noncanonical Wnt pathways. These signalling loops contribute to the CSC properties of cells with an active EMT programme. BMPs, bone morphogenetic proteins; DKK1, Dickkopf-related protein 1; FLPs, filopodium-like protrusions; SFRP1, secreted Frizzled-related protein 1. Shibue, T. & Weinberg, R. A. (2017) EMT, CSCs, and drug resistance: the mechanistic link and clinical implications Nat. Rev. Clin. Oncol. doi:10.1038/nrclinonc.2017.44