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Distinguishing mechanisms underlying EMT tristability.

Dongya Jia1,2, Mohit Kumar Jolly1,3, Satyendra C Tripathi4

  • 11Center for Theoretical Biological Physics, Rice University, Houston, TX 77005 USA.

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|April 7, 2018
PubMed
Summary

The Epithelial-Mesenchymal Transition (EMT) involves distinct cell phenotypes. Experimental data supports the ternary chimera switch model for EMT regulation, highlighting miR-200/ZEB1

Keywords:
CBSCascading bistable switchesEMTEpithelial-Mesenchymal transitionFOXC2TCSTernary chimera switchZEB1

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Area of Science:

  • Cell biology
  • Cancer research
  • Systems biology

Background:

  • Epithelial-Mesenchymal Transition (EMT) is crucial for development and cancer metastasis.
  • EMT involves transitions between epithelial (E), hybrid epithelial/mesenchymal (E/M), and mesenchymal (M) phenotypes.
  • The miR-34/SNAIL/miR-200/ZEB1 network is central to EMT, but its dynamics are debated.

Purpose of the Study:

  • To evaluate two mathematical models (TCS and CBS) of the EMT regulatory network.
  • To reconcile theoretical models with experimental observations of EMT dynamics.
  • To determine how the miR-200/ZEB1 module governs transitions between E, E/M, and M phenotypes.

Main Methods:

  • Integrated experimental and theoretical approach.
  • Analysis of SNAIL and ZEB1 responses to TGF-β.
  • Experimental manipulation of SNAIL, ZEB1, and FOXC2 in cell lines (H1975, HMLE).

Main Results:

  • Both TCS and CBS models explain the two-step EMT (E→E/M→M) and TGF-β responses.
  • ZEB1 levels are intermediate in hybrid E/M cells.
  • SNAIL overexpression alone does not induce EMT without ZEB1 and FOXC2.

Conclusions:

  • Experimental findings favor the ternary chimera switch (TCS) model.
  • The miR-200/ZEB1 pathway acts as a three-way switch for EMT phenotype transitions.