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Review
. 2012 Oct;22(5-6):411-6.
doi: 10.1016/j.semcancer.2012.04.008. Epub 2012 Apr 30.

Epithelial to mesenchymal transition: new and old insights from the classical neural crest model

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Review

Epithelial to mesenchymal transition: new and old insights from the classical neural crest model

Pablo H Strobl-Mazzulla et al. Semin Cancer Biol. 2012 Oct.

Abstract

The epithelial-to-mesenchymal transition (EMT) is an important event converting compact and ordered epithelial cells into migratory mesenchymal cells. Given the molecular and cellular similarities between pathological and developmental EMTs, studying this event during neural crest development offers and excellent in vivo model for understanding the mechanisms underlying this process. Here, we review new and old insight into neural crest EMT in search of commonalities with cancer progression that might aid in the design of specific therapeutic prevention.

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Conflict of interest statement

Conflict of interest statement

The authors declare there are no conflicts of interest.

Figures

Figure 1
Figure 1
(A) Schematic representation of the genes expressed on neural crest cells prior (green) and after (red) undergoes epithelial-to-mesenchymal transition. (B) Neural crest epithelial-to-mesenchymal transition regulation. NC specifiers, FoxD3 and Snail down-regulate expression of molecules that are associated with epithelial static cell populations, such as N-Cad and E-Cad (or Cad6B in chick and mouse), respectively, to give place to the up-regulation of mesenchymal migratory proteins, such as Cad7. Similarly, Snail down-regulates tight junction claudins/occludins to permit the upregulation of gap junction protein connexin-43α1 (Cx43α1), which may also depend on Snail expression. Gene regulation in which the repressors Snail or FoxD3 up-regulate the expression of matrix metalloproteases (MMPs), integrins, Cad7 or RhoB may denote indirect regulatory interactions, possibly mediated by other repressors (represented by dotted lines).

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