Carcinomas are phenotypically arrayed along an epithelial–mesenchymal transition (EMT) spectrum, a developmental program currently exploited to understand the acquisition of drug resistance through a re-routing of growth factor signaling. This review collates the current approaches employed in developing therapeutics against cancer-associated EMT, and provides an assessment of their respective strengths and drawbacks. We reflect on the close relationship between EMT and chemoresistance against current targeted therapeutics, with a special focus on the epigenetic mechanisms that link these processes. This prompts the hypothesis that carcinoma-associated EMT shares a common epigenetic pathway to cellular plasticity as somatic cell reprogramming during tissue repair and regeneration. Indeed, their striking resemblance suggests that EMT in carcinoma is a pathological adaptation of an intrinsic program of cellular plasticity that is crucial to tissue homeostasis. We thus propose a revised approach that targets the epigenetic mechanisms underlying pathogenic EMT to arrest cellular plasticity regardless of upstream cancer-driving mutations.
CITATION STYLE
Voon, D. C., Huang, R. Y., Jackson, R. A., & Thiery, J. P. (2017, July 1). The EMT spectrum and therapeutic opportunities. Molecular Oncology. Wiley Blackwell. https://doi.org/10.1002/1878-0261.12082
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