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. 2011 Jan 24;192(2):209–218. doi: 10.1083/jcb.201009059

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© 2011 Muller et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 1. — p53 opposes EMT and cell migration to prevent metastasis. p53 plays a role in opposing EMT and cell migration. A hallmark of EMT is loss of E-cadherin, and p53 can prevent this by inhibiting Slug or the adhesion molecule EpCam expression. Furthermore, loss of p53 or decreased p53 activity after Twist expression can therefore drive EMT. p53 can also inhibit invasive migration. This can be mediated via increased expression of Caldesmon or miRNA-143 to oppose invadopodia formation. By transactivating PTEN, p53 can reduce PIP3 (and thereby Rac) levels, resulting in inhibition of mesenchymal/elongated motility. p53 can also inhibit amoeboid cell motility by preventing activation of ROCK, either by inducing Notch or by promoting RhoE (Rnd3)-mediated inhibition of RhoA. E-CAD, E-cadherin.