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A microRNA gene expression signature predicts response to erlotinib in epithelial cancer cell lines and targets EMT

J L Bryant1, J Britson, J M Balko

  • 1Department of Pharmaceutical Sciences, College of Pharmacy, 343 Bio-Pharm Complex, University of Kentucky, Lexington, KY 40536-0082, USA.

British Journal of Cancer
|November 3, 2011
PubMed
Abstract

Insights

MicroRNA (miRNA) gene expression predicts response to epidermal growth factor receptor (EGFR) inhibitors in non-small-cell lung cancer. This miRNA signature is linked to epithelial-to-mesenchymal transition (EMT), driving resistance and metastasis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Epidermal growth factor receptor (EGFR) inhibitors show efficacy in non-small-cell lung cancer (NSCLC) and pancreatic ductal adenocarcinoma (PDAC).
  • Predictive biomarkers for EGFR inhibitor response include EGFR/KRAS mutation status, EGFR amplification, and gene expression profiles.

Purpose of the Study:

  • To identify microRNA (miRNA) gene expression signatures that predict response to EGFR inhibition in NSCLC.
  • To investigate the relationship between miRNA expression, epithelial-to-mesenchymal transition (EMT), and EGFR inhibitor sensitivity.

Main Methods:

  • Utilized an NSCLC cell line model system to identify and characterize predictive miRNA gene expression.
  • Analyzed miRNA expression in cancer cell lines and tumors to correlate with EGFR inhibitor response and metastatic status.

Main Results:

  • A 13-miRNA gene signature was identified, predicting response to EGFR inhibition and distinguishing primary from metastatic tumors.
  • Signature miRNAs target proteins enriched in epithelial-to-mesenchymal transition (EMT) pathways, which are associated with EGFR inhibitor resistance and metastasis.
  • Altered expression of the EMT transcription factor ZEB1 and upregulation of signature miRNAs were observed in erlotinib-sensitive NSCLC and PDAC; mir-200c ectopic expression affected EMT, erlotinib sensitivity, and migration.

Conclusions:

  • Hypothesize that tumor microenvironment-induced TGFβ1 stimulates a miRNA program driving resistance to anti-EGFR therapy.
  • This miRNA program promotes EMT, invasion, and metastasis in lung tumor cells, contributing to therapeutic resistance.

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