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The Emerging Roles of RUNX Transcription Factors in Epithelial-Mesenchymal Transition

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RUNX Proteins in Development and Cancer

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 962))

Abstract

Epithelial-mesenchymal transition (EMT) is an evolutionary conserved morphogenetic program necessary for the shaping of the body plan during development. It is guided precisely by growth factor signaling and a dedicated network of specialised transcription factors. These are supported by other transcription factor families serving auxiliary functions during EMT, beyond their general roles as effectors of major signaling pathways. EMT transiently induces in epithelial cells mesenchymal properties, such as the loss of cell-cell adhesion and a gain in cell motility. Together, these newly acquired properties enable their migration to distant sites where they eventually give rise to adult epithelia. However, it is now recognized that EMT contributes to the pathogenesis of several human diseases, notably in tissue fibrosis and cancer metastasis. The RUNX family of transcription factors are important players in cell fate determination during development, where their spatio-temporal expression often overlaps with the occurrence of EMT. Furthermore, the dysregulation of RUNX expression and functions are increasingly linked to the aberrant induction of EMT in cancer. The present chapter reviews the current knowledge of this emerging field and the common themes of RUNX involvement during EMT, with the intention of fostering future research.

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Acknowledgement

The authors thank Rebecca Jackson for her generous help in the preparation of the manuscript. We are also grateful to Jormay Lim and Isao Kobayashi for their valuable input.

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Voon, D.CC., Thiery, J.P. (2017). The Emerging Roles of RUNX Transcription Factors in Epithelial-Mesenchymal Transition. In: Groner, Y., Ito, Y., Liu, P., Neil, J., Speck, N., van Wijnen, A. (eds) RUNX Proteins in Development and Cancer. Advances in Experimental Medicine and Biology, vol 962. Springer, Singapore. https://doi.org/10.1007/978-981-10-3233-2_28

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