TGF-beta and epithelial-to-mesenchymal transitions

Oncogene. 2005 Aug 29;24(37):5764-74. doi: 10.1038/sj.onc.1208927.


Remarkable phenotype plasticity of epithelial cells underlies morphogenesis, epithelial repair and tumor invasiveness. Detailed understanding of the contextual cues and molecular mediators that control epithelial plasticity will be required in order to develop viable therapeutic approaches targeting epithelial-to-mesenchymal transition (EMT), an advanced manifestation of epithelial plasticity. Members of the transforming growth factor (TGF-beta) family of growth factors can initiate and maintain EMT in a variety of biological systems and pathophysiological context by activating major signaling pathways and transcriptional regulators integrated in extensive signaling networks. Here we will review the distinct physiological contexts of EMT and the underlying molecular signaling networks controlled by TGF-beta.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Cell Adhesion
  • Cell Differentiation*
  • Cell Polarity
  • Cytoskeleton / physiology
  • DNA-Binding Proteins / physiology
  • Epithelial Cells / cytology*
  • Extracellular Signal-Regulated MAP Kinases / physiology
  • Gene Expression Regulation
  • Humans
  • Mesoderm / cytology*
  • Nuclear Proteins / physiology
  • Phenotype
  • Signal Transduction
  • Smad Proteins
  • Snail Family Transcription Factors
  • Trans-Activators / physiology
  • Transcription Factors / physiology
  • Transforming Growth Factor beta / physiology*
  • Twist-Related Protein 1


  • DNA-Binding Proteins
  • Nuclear Proteins
  • Smad Proteins
  • Snail Family Transcription Factors
  • TWIST1 protein, human
  • Trans-Activators
  • Transcription Factors
  • Transforming Growth Factor beta
  • Twist-Related Protein 1
  • Extracellular Signal-Regulated MAP Kinases