Stem-cell-like properties and epithelial plasticity arise as stable traits after transient Twist1 activation

Cell Rep. 2015 Jan 13;10(2):131-9. doi: 10.1016/j.celrep.2014.12.032. Epub 2015 Jan 8.

Abstract

Master regulators of the epithelial-mesenchymal transition such as Twist1 and Snail1 have been implicated in invasiveness and the generation of cancer stem cells, but their persistent activity inhibits stem-cell-like properties and the outgrowth of disseminated cancer cells into macroscopic metastases. Here, we show that Twist1 activation primes a subset of mammary epithelial cells for stem-cell-like properties, which only emerge and stably persist following Twist1 deactivation. Consequently, when cells undergo a mesenchymal-epithelial transition (MET), they do not return to their original epithelial cell state, evidenced by acquisition of invasive growth behavior and a distinct gene expression profile. These data provide an explanation for how transient Twist1 activation may promote all steps of the metastatic cascade; i.e., invasion, dissemination, and metastatic outgrowth at distant sites.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents, Hormonal / pharmacology
  • Breast Neoplasms / metabolism
  • Breast Neoplasms / pathology
  • Cell Culture Techniques
  • Cell Line
  • Cell Movement / drug effects
  • Cell Proliferation / drug effects
  • Epithelial Cells / cytology
  • Epithelial Cells / metabolism
  • Epithelial-Mesenchymal Transition / drug effects
  • Female
  • Humans
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism*
  • Snail Family Transcription Factors
  • Stem Cells / cytology
  • Stem Cells / metabolism
  • Tamoxifen / pharmacology
  • Transcription Factors / genetics
  • Transcription Factors / metabolism
  • Twist-Related Protein 1 / genetics
  • Twist-Related Protein 1 / metabolism*

Substances

  • Antineoplastic Agents, Hormonal
  • Nuclear Proteins
  • SNAI1 protein, human
  • Snail Family Transcription Factors
  • TWIST1 protein, human
  • Transcription Factors
  • Twist-Related Protein 1
  • Tamoxifen