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Updated: Jul 14, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

Human RON receptor tyrosine kinase induces complete epithelial-to-mesenchymal transition but causes cellular

Marceline Côté1, A Dusty Miller, Shan-Lu Liu

  • 1Department of Microbiology and Immunology, McGill University, Montreal, Canada.

Biochemical and Biophysical Research Communications
|June 26, 2007
PubMed

Insights

Overexpressing the RON receptor tyrosine kinase in epithelial cells induces complete epithelial-to-mesenchymal transition (EMT). However, high RON levels unexpectedly cause cell cycle arrest and senescence, impairing proliferation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • The RON receptor tyrosine kinase (RTK) is a MET proto-oncogene family member crucial for cell functions and cancer.
  • Its role in epithelial-to-mesenchymal transition (EMT) and cell proliferation requires further elucidation.

Purpose of the Study:

  • To investigate the biological effects of varying RON expression levels in Madin-Darby canine kidney (MDCK) epithelial cells.
  • To determine if RON overexpression drives cell transformation or other cellular processes.

Main Methods:

  • Generation of MDCK cell clones with differential RON expression.
  • Analysis of cell morphology, proliferation, motility, invasiveness, and signaling pathways.
  • Assessment of RON tyrosine phosphorylation and MAPK pathway activation.

Main Results:

  • High RON expression induced complete and stabilized EMT, characterized by morphological scattering and increased motility/invasiveness.
  • Unexpectedly, high RON levels led to retarded proliferation, cell cycle arrest, and senescence.
  • Constitutive RON tyrosine phosphorylation and MAPK pathway activation were observed in high-RON expressing, EMT-positive cells.

Conclusions:

  • RON is sufficient to induce complete and stabilized EMT in MDCK cells.
  • RON overexpression does not cause cell transformation but rather induces senescence and impairs proliferation.
  • These findings highlight a complex role for RON in epithelial cell biology and cancer progression.

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