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Oncogenic roles of EMT-inducing transcription factors

Abstract

The plasticity of cancer cells underlies their capacity to adapt to the selective pressures they encounter during tumour development. Aberrant reactivation of epithelial–mesenchymal transition (EMT), an essential embryonic process, can promote cancer cell plasticity and fuel both tumour initiation and metastatic spread. Here we discuss the roles of EMT-inducing transcription factors in creating a pro-tumorigenic setting characterized by an intrinsic ability to withstand oncogenic insults through the mitigation of p53-dependent oncosuppressive functions and the gain of stemness-related properties.

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Figure 1: Schematic overview of EMT pathways.
Figure 2: Inhibition of tumour-suppressive programs by EMT-TFs.
Figure 3: Crosstalk between EMT-TFs, p53 and RB pathways and stemness factors in regulating cancer cell plasticity.

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Acknowledgements

We thank members of the Puisieux and Brabletz laboratories for helpful discussions and Sarah Kabani for critical reading of the manuscript. A.P. is supported by grants from the Ligue Nationale contre le Cancer, the Association pour la Recherche contre le Cancer (ARC), the Institut National du Cancer (PLBI009), the Lyon integrated Research Institute in Cancer (LYRIC) and the LabEx DEVweCAN (ANR-10-LABX-0061) of Lyon University, within the program 'Investissements d'Avenir' (ANR-11-IDEX-0007) operated by the French National Research Agency (ANR). A.P. is a member of the Institut Universitaire de France. T.B. is supported by the DFG (BR1399/6-1; SFB850,B2 and SFB992,C06) and the Deutsche Krebshilfe (grant no. 109430).

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Puisieux, A., Brabletz, T. & Caramel, J. Oncogenic roles of EMT-inducing transcription factors. Nat Cell Biol 16, 488–494 (2014). https://doi.org/10.1038/ncb2976

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