AKT primes snail-induced EMT concomitantly with the collective migration of squamous cell carcinoma cells

J Cell Biochem. 2013 Sep;114(9):2039-49. doi: 10.1002/jcb.24545.

Abstract

In this study, we found that wounding of a confluent monolayer of squamous cell carcinoma (SCC) cells induced epithelial-mesenchymal transition (EMT) specifically at the edge of the wound. This process required the combined stimulation of TGFβ, TNFα, and PDGF-D. Such a combined cytokine treatment of confluent monolayers of the cells upregulated the expression levels of Snail and Slug via PI3K. The PI3K downstream effector, AKT, was dispensable for the upregulation of Snail and Slug, but essential for enabling EMT in response to upregulation of Snail and Slug.

Keywords: AKT; EMT; PI3K; SNAIL; SQUAMOUS CELL CARCINOMA.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinoma, Squamous Cell / metabolism*
  • Cell Line
  • Cell Movement / genetics
  • Cell Movement / physiology
  • Epithelial-Mesenchymal Transition / genetics
  • Epithelial-Mesenchymal Transition / physiology*
  • Humans
  • Immunoblotting
  • Immunohistochemistry
  • Lymphokines / metabolism
  • Phosphatidylinositol 3-Kinases / genetics
  • Phosphatidylinositol 3-Kinases / metabolism
  • Platelet-Derived Growth Factor / metabolism
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Snail Family Transcription Factors
  • Transcription Factors / metabolism*
  • Transforming Growth Factor beta / metabolism
  • Tumor Necrosis Factor-alpha / metabolism
  • Wound Healing / genetics
  • Wound Healing / physiology

Substances

  • Lymphokines
  • PDGFD protein, human
  • Platelet-Derived Growth Factor
  • SNAI1 protein, human
  • Snail Family Transcription Factors
  • Transcription Factors
  • Transforming Growth Factor beta
  • Tumor Necrosis Factor-alpha
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt