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Restoring E-cadherin expression increases sensitivity to epidermal growth factor receptor inhibitors in lung cancer

Samir E Witta1, Robert M Gemmill, Fred R Hirsch

  • 1Department of Medicine/Medical Oncology, University of Colorado Health Sciences Center and University of Colorado Cancer Center, Campus Box 8117, PO Box 6511, Aurora, CO 80045, USA. Samir.Witta@uchsc.edu

Cancer Research
|January 21, 2006
PubMed

Insights

This study reveals E-cadherin and ZEB1 expression predict response to epidermal growth factor receptor (EGFR) inhibitors in non-small cell lung cancer (NSCLC). Combining HDAC inhibitors with EGFR inhibitors may overcome treatment resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Epidermal growth factor receptor (EGFR) is overexpressed in most non-small cell lung cancers (NSCLC).
  • EGFR tyrosine kinase inhibitors (TKIs) like gefitinib show limited response rates in NSCLC patients.
  • E-Cadherin and ZEB1 are implicated in NSCLC progression and EGFR signaling.

Purpose of the Study:

  • To investigate the predictive value of E-cadherin and ZEB1 expression for gefitinib sensitivity in NSCLC.
  • To explore the potential of combined HDAC inhibition and gefitinib treatment to overcome TKI resistance.

Main Methods:

  • Correlation analysis between gefitinib sensitivity and E-cadherin/ZEB1 expression.
  • E-Cadherin transfection into gefitinib-resistant NSCLC cell lines.
  • Treatment of resistant cell lines with HDAC inhibitor MS-275 and gefitinib.

Main Results:

  • Significant correlation found between gefitinib sensitivity and E-cadherin/ZEB1 expression.
  • E-Cadherin transfection restored gefitinib sensitivity in resistant cells.
  • Combined MS-275 and gefitinib treatment induced apoptosis and growth inhibition in resistant cells, mimicking sensitive cell lines.

Conclusions:

  • E-Cadherin and ZEB1 expression can predict responsiveness to EGFR-TKIs in NSCLC.
  • Combined HDAC inhibitor and gefitinib treatment is a promising strategy to overcome resistance to EGFR inhibitors in lung cancer.

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