Chapter 6
EMT: An Update
Jean Paul Thiery
Abstract
Epithelial Mesenchymal Transition (EMT) initially discovered as a key developmental mechanism is now
shown to be indirectly involved in fibrosis and is contributing to the progression of carcinomas. Additionally, to transcription factors driving the morphological transition, novel mechanisms are now described to
modulate the different features of the transition. The debate as to whether EMT is essential for the
dissemination of carcinoma cells from the primary tumors is likely to be resolved soon, considering that
EMT is not a linear transition from an epithelial to a mesenchymal state. Multiple intermediate states can be
reached without involving the presence of some of known transcription factors initially described as
indispensable for the acquisition of mesenchymal-like phenotypes.
Key words Epithelial-to-mesenchymal transition, Morphogenesis, Gastrulation, Cancer, Fibrosis,
EMT spectrum, Ribosome biogenesis, Stemness
Epithelial Mesenchymal Transition (EMT) designates a fundamental process driving morphogenesis and organogenesis in multicellular organisms. During gastrulation, the primitive epithelium
undergoes a drastic morphological transition, engaging presumptive mesodermal and endodermal cells into a migratory behavior
through the transient or permanent loss of apico-basal polarity of
epithelial cells and the acquisition of front-rear polarity in newly
formed mesenchymal cells. The reverse mechanism, Mesenchymal
Epithelial Transition (MET), is critically important to resume an
epithelial state during subsequent stages of morphogenesis and in
organogenesis. MET is a mandatory step in the newly formed
mesenchyme to generate somites, precursors of the vertebrae, and
the kidney. Heart development also involves cycles of EMT and
MET [1].
EMT is actively studied in embryonic development. Gene regulatory networks during gastrulation in Drosophila melanogaster,
the sea urchin, and in the neural crest of vertebrates have been
partially elucidated [2, 3]. Mechanisms driving gastrulation and
neural crest ontogeny share transcriptional regulation, particularly
Kyra Campbell and Eric Theveneau (eds.), The Epithelial-to Mesenchymal Transition: Methods and Protocols,
Methods in Molecular Biology, vol. 2179, https://doi.org/10.1007/978-1-0716-0779-4_6,
© Springer Science+Business Media, LLC, part of Springer Nature 2021
35
EMT: An Update
Jean Paul Thiery
Abstract
Epithelial Mesenchymal Transition (EMT) initially discovered as a key developmental mechanism is now
shown to be indirectly involved in fibrosis and is contributing to the progression of carcinomas. Additionally, to transcription factors driving the morphological transition, novel mechanisms are now described to
modulate the different features of the transition. The debate as to whether EMT is essential for the
dissemination of carcinoma cells from the primary tumors is likely to be resolved soon, considering that
EMT is not a linear transition from an epithelial to a mesenchymal state. Multiple intermediate states can be
reached without involving the presence of some of known transcription factors initially described as
indispensable for the acquisition of mesenchymal-like phenotypes.
Key words Epithelial-to-mesenchymal transition, Morphogenesis, Gastrulation, Cancer, Fibrosis,
EMT spectrum, Ribosome biogenesis, Stemness
Epithelial Mesenchymal Transition (EMT) designates a fundamental process driving morphogenesis and organogenesis in multicellular organisms. During gastrulation, the primitive epithelium
undergoes a drastic morphological transition, engaging presumptive mesodermal and endodermal cells into a migratory behavior
through the transient or permanent loss of apico-basal polarity of
epithelial cells and the acquisition of front-rear polarity in newly
formed mesenchymal cells. The reverse mechanism, Mesenchymal
Epithelial Transition (MET), is critically important to resume an
epithelial state during subsequent stages of morphogenesis and in
organogenesis. MET is a mandatory step in the newly formed
mesenchyme to generate somites, precursors of the vertebrae, and
the kidney. Heart development also involves cycles of EMT and
MET [1].
EMT is actively studied in embryonic development. Gene regulatory networks during gastrulation in Drosophila melanogaster,
the sea urchin, and in the neural crest of vertebrates have been
partially elucidated [2, 3]. Mechanisms driving gastrulation and
neural crest ontogeny share transcriptional regulation, particularly
Kyra Campbell and Eric Theveneau (eds.), The Epithelial-to Mesenchymal Transition: Methods and Protocols,
Methods in Molecular Biology, vol. 2179, https://doi.org/10.1007/978-1-0716-0779-4_6,
© Springer Science+Business Media, LLC, part of Springer Nature 2021
35