Abstract
A major transcriptional and phenotypic reprogramming event during development is the establishment of the mesodermal layer from the ectoderm through epithelial-mesenchymal transition (EMT). EMT is employed in subsequent developmental events, and also in many physiological and pathological processes, such as the dissemination of cancer cells through metastasis, as a reversible transition between epithelial and mesenchymal states. The remarkable phenotypic remodeling accompanying these transitions is driven by characteristic transcription factors whose activities and/or activation depend upon signaling cues and co-factors, including intermediary metabolites. In this review, we summarize salient metabolic features that enable or instigate these transitions, as well as adaptations undergone by cells to meet the metabolic requirements of their new states, with an emphasis on the roles played by the metabolic regulation of epigenetic modifications, notably methylation and acetylation.
Highlights
Cells undergoing switches from epithelial to mesenchymal states experience radical changes in motility, proliferation, morphology and interactions with their environment
In cancer, transformed cells endowed with phenotypic plasticity co-opt these same mechanisms as they evolve and adapt in response to environmental challenges, yielding intratumoral heterogeneity, which significantly impacts the biology and management of cancers
Epithelial-mesenchymal plasticity is so deeply intertwined with metabolic reprogramming that the two processes may no longer be considered separately, in physiological or pathological scenarios
Summary
Cells undergoing switches from epithelial to mesenchymal states experience radical changes in motility, proliferation, morphology and interactions with their environment. They adjust their rate of proliferation to the degree of motility, such that highly motile cells with strong acquired mesenchymal phenotypes may exhibit a diminished proliferative potential [2], while cells at “intermediate” states of EMT may retain or increase their proliferation rates relative to their initial epithelial states [3]. This suggests a balance between motility and proliferation [4,5], that may depend on the relative availability of common resources that can be spent on either motility or on proliferation. We will review relevant interconnections between EMT and metabolism, with a particular emphasis on the modulation by metabolites of epigenetic readouts, including EMT
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
