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Failsafe program escape and EMT: a deleterious partnership

Stéphane Ansieau1, Stéphanie Courtois-Cox, Anne-Pierre Morel

  • 1Inserm UMR-S1052, Centre de Recherche en Cancérologie, Lyon F-69008, France. stephane.ansieau@lyon.unicancer.fr

Seminars in Cancer Biology
|October 12, 2011
PubMed

Insights

The epithelial to mesenchymal transition (EMT) process, when reactivated, drives tumor metastasis and initiation by neutralizing RB and p53 pathways. This review explores the link between EMT, senescence, apoptosis, and tumor development.

Area of Science:

  • Oncology
  • Cell Biology
  • Developmental Biology

Background:

  • Epithelial to mesenchymal transition (EMT) is an embryonic process reactivated in cancer, promoting metastasis.
  • EMT inducers are linked to escaping senescence and apoptosis, suggesting a role in tumor initiation.
  • Oncogenic potential of EMT involves neutralizing RB and p53 tumor suppressor pathways.

Purpose of the Study:

  • To explore the interlink between EMT and cell safety programs (RB/p53 pathways).
  • To understand how this crosstalk facilitates cell transformation and tumor initiation.

Main Methods:

  • Literature review and synthesis of existing research on EMT, RB, and p53 pathways.
  • Analysis of the molecular mechanisms underlying EMT induction and its interaction with cell cycle and apoptosis regulation.

Main Results:

  • EMT inducers can override senescence and apoptosis.
  • EMT inducers neutralize RB and p53, crucial for maintaining epithelial state.
  • Unexpected crosstalk exists between EMT and cellular safety mechanisms.

Conclusions:

  • Aberrant EMT contributes to both tumor initiation and progression.
  • Understanding the EMT-RB/p53 interplay is key to comprehending cell transformation and tumorigenesis.

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