Snail family members unequally trigger EMT and thereby differ in their ability to promote the neoplastic transformation of mammary epithelial cells

PLoS One. 2014 Mar 17;9(3):e92254. doi: 10.1371/journal.pone.0092254. eCollection 2014.

Abstract

By fostering cell commitment to the epithelial-to-mesenchymal transition (EMT), SNAIL proteins endow cells with motility, thereby favoring the metastatic spread of tumor cells. Whether the phenotypic change additionally facilitates tumor initiation has never been addressed. Here we demonstrate that when a SNAIL protein is ectopically produced in non-transformed mammary epithelial cells, the cells are protected from anoikis and proliferate under low-adherence conditions: a hallmark of cancer cells. The three SNAIL proteins show unequal oncogenic potential, strictly correlating with their ability to promote EMT. SNAIL3 especially behaves as a poor EMT-inducer comforting the concept that the transcription factor functionally diverges from its two related proteins.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Breast Neoplasms / genetics
  • Breast Neoplasms / pathology
  • Cell Adhesion / genetics
  • Cell Survival / genetics
  • Cell Transformation, Neoplastic / genetics
  • Cell Transformation, Neoplastic / pathology*
  • Epithelial Cells / metabolism*
  • Epithelial Cells / pathology*
  • Epithelial-Mesenchymal Transition* / genetics
  • Female
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Mammary Glands, Human / pathology*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Snail Family Transcription Factors
  • Telomerase / metabolism
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*

Substances

  • RNA, Messenger
  • Snail Family Transcription Factors
  • Transcription Factors
  • Telomerase

Grants and funding

This work was financially supported by the Association pour la Recherche contre le Cancer and was performed within the framework of the LABEX DEVweCAN (ANR-10-LABX-0061 of Lyon University, within the program “Investissements d'Avenir (ANR-11-IDEX 0007) operated by the French National Agency (ANR). BG received support from the Ministère de la Recherche and the Fondation des Treilles. LJ is a recipient of fellowships from the Ligue Nationale Contre le Cancer. The funders had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript.