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Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure
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EMT-Mediated Acquired EGFR-TKI Resistance in NSCLC: Mechanisms and Strategies

Xuan Zhu1,2, Lijie Chen3, Ling Liu4

  • 1Institute of Translational Medicine, China Medical University, Shenyang, China.

Frontiers in Oncology
|November 5, 2019
PubMed

Insights

Acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) is a major challenge in non-small-cell lung cancer (NSCLC). Understanding the epithelial-mesenchymal transition (EMT) mechanism is key to overcoming EGFR-TKI resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are standard treatments for non-small-cell lung cancer (NSCLC) harboring specific mutations.
  • Acquired resistance to EGFR-TKIs significantly limits their long-term efficacy, posing a critical challenge in clinical practice.
  • The epithelial-mesenchymal transition (EMT) is increasingly recognized as a key mechanism driving acquired resistance to targeted cancer therapies.

Purpose of the Study:

  • To elucidate the mechanistic role of EMT in the acquisition of EGFR-TKI resistance in NSCLC.
  • To provide a comprehensive framework for understanding EMT-mediated resistance.
  • To explore potential therapeutic strategies to overcome EMT-driven EGFR-TKI resistance in NSCLC.

Main Methods:

  • Review and synthesis of current literature on EGFR-TKI resistance and EMT in NSCLC.
  • Mechanistic analysis of biological pathways involved in EMT and drug resistance.
  • Discussion of emerging therapeutic strategies targeting EMT.

Main Results:

  • EMT is a significant contributor to acquired resistance to EGFR-TKIs in NSCLC.
  • Specific molecular pathways driving EMT can be targeted to re-sensitize tumors to EGFR-TKIs.
  • Understanding the dynamic nature of EMT is crucial for developing effective treatment strategies.

Conclusions:

  • EMT represents a critical mechanism underlying EGFR-TKI resistance in NSCLC.
  • Targeting EMT pathways offers a promising therapeutic avenue to overcome acquired resistance.
  • Further research into EMT-targeted therapies is warranted to improve clinical outcomes for NSCLC patients.
Keywords:
acquired resistanceepidermal growth factor receptor tyrosine kinase inhibitorsepithelial-mesenchymal transitionnon-small-cell lung cancertherapeutic strategies

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