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Updated: Aug 5, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

Early-Phase Activation of Epithelial-Mesenchymal Transition in Lung Cancer Cells Treated with Epidermal Growth Factor

Alessia Belloni1, Lorenza Tamberi1, Laura Graciotti2

  • 1Department of Clinical and Molecular Sciences (DISCLIMO), Polytechnic University of Marche, 60121 Ancona, Italy.

International Journal of Molecular Sciences
|July 28, 2026
PubMed

Insights

Epithelial-mesenchymal transition (EMT) markers like E-cadherin and N-cadherin change during EGFR tyrosine kinase inhibitor (TKI) treatment in lung cancer. Slug expression increases, suggesting EMT

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Epithelial-mesenchymal transition (EMT) is linked to resistance against epidermal growth factor receptor tyrosine kinase inhibitors (TKIs).
  • Key EMT markers include E-cadherin loss, N-cadherin and vimentin increase, and transcription factors like Snail, Slug, Zeb1, Zeb2, and Twist.
  • Understanding EMT mechanisms is crucial for overcoming TKI resistance in lung cancer.

Purpose of the Study:

  • To investigate the expression of EMT markers in lung cancer cell lines with wild-type and mutated epidermal growth factor receptors (EGFR).
  • To determine the role of EMT in the early stages of TKI treatment using Gefitinib or Osimetinib, with or without TGF-β.
  • To analyze changes in E-cadherin, N-cadherin, vimentin, and transcription factor expression at 24 and 96 hours post-treatment.

Main Methods:

  • Utilized lung cancer cell lines A549 (wild-type EGFR) and PC9 (mutated EGFR).
  • Treated PC9 cells with Gefitinib or Osimetinib, alone and in combination with TGF-β.
  • Assessed expression of EMT markers (E-cadherin, N-cadherin, vimentin) and transcription factors (Slug) at 24h and 96h timepoints.

Main Results:

  • Gefitinib or Osimertinib treatment in PC9 cells induced E-cadherin reduction and N-cadherin increase by 96 hours, irrespective of TGF-β.
  • These changes mimicked TGF-β-induced effects in A549 cells at 24 hours.
  • Slug expression significantly increased in PC9 cells treated with Gefitinib or Osimertinib at 96 hours.

Conclusions:

  • Changes in EMT markers during early TKI treatment suggest a role in facilitating drug resistance.
  • Slug upregulation is a key event in TKI-treated lung cancer cells exhibiting EMT characteristics.
  • Targeting EMT pathways may offer strategies to overcome TKI resistance in EGFR-mutated lung cancers.
Keywords:
epithelial-to-mesenchymal transitiongefitinibnon-small cell lung cancerosimertinibtyrosine kinase inhibitors

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