Epithelial-mesenchymal transition

Epithelial-mesenchymal transition (EMT) is a developmental program characterized by loss of celladhesion, repression of E-cadherin expression, and increased cell mobility. EMT is essential for numerous developmental processes including mesodermformation and neural tube formation.

Several signal transduction pathways, such as Ras-MAPK and Wnt, have been shown to be involved in regulation of EMT. In particular, Ras-MAPK has been shown to activate two related transcription factorsknown as Snail and Slug. Both of these proteins are transcriptional repressors of E-cadherin and their expression induces EMT. Twist, another transcription factor, has also been shown to induce EMT, and is also implicated in the regulation of metastasis.

Initiation of metastasisinvolves invasion, which has many phenotypic similarities to EMT, including a loss of cell-cell adhesion mediated by E-cadherin repression and an increase in cell mobility.

Sources

Vernon, A., and LaBonne, C. (2004). Tumor metastasis: a new twist on epithelial-mesenchymal transitions. Current Biology. 14, 719-721.

Yang, J., Mani, S., Donaher, J., Ramaswamy, S., Itzkyson, R., Come, C., Savagner, P., Gitelman, I., Richardson, A., and Weinberg, R. (2004). Twist, a master regulator of morphogenesis, plays an essential role in tumor metastasis. Cell. 117, 927-939.

This article is licensed under the GNU Free Documentation License.
It uses material from the http://en.wikipedia.org/wiki/Epithelial-mesenchymal+transition Wikipedia article Epithelial-mesenchymal transition.