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EGFR-TKI resistance and MAP17 are associated with cancer stem cell like properties

Yi Shao1, Hui Lv1, Dian-Sheng Zhong1

  • 1Department of Oncology, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.

Oncology Letters
|April 5, 2018
PubMed

Insights

Cancer stem cells (CSCs) contribute to resistance against epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) in non-small-cell lung cancer. MAP17 overexpression in CSCs is linked to this TKI resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Acquired resistance to tyrosine kinase inhibitors (TKIs) is a significant challenge in treating non-small-cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) mutations.
  • Cancer stem cells (CSCs) are increasingly implicated in therapeutic resistance.
  • The role of MAP17 in CSCs and its contribution to TKI resistance in NSCLC remain largely unexplored.

Purpose of the Study:

  • To investigate the influence of CSC-like cells on TKI resistance in EGFR-mutant NSCLC.
  • To elucidate the potential role of MAP17 in CSCs within the context of TKI resistance.

Main Methods:

  • Cultured EGFR-mutant NSCLC cell line (PC9) under serum-deprived conditions to enrich for CSC-like cells.
  • Assessed CSC properties including stem cell marker expression (CD133, CD44, Oct-4, ABCG2), self-renewal, invasion, proliferation, and tumorigenesis.
  • Compared MAP17 expression levels between sphere (CSC-like) and parent cells.
  • Investigated the functional association of MAP17 with self-renewal, TKI resistance, and Na-dependent glucose transporter 1.

Main Results:

  • Enriched CSC-like cells exhibited stem cell phenotypes and acquired resistance to erlotinib.
  • Sphere cells demonstrated significantly higher MAP17 expression compared to parent cells.
  • MAP17 expression positively correlated with CSC self-renewal capacity and erlotinib resistance.
  • MAP17's function in TKI resistance was partially dependent on the Na-dependent glucose transporter 1.

Conclusions:

  • CSC-like cells contribute to erlotinib resistance in EGFR-mutant NSCLC.
  • MAP17 is overexpressed in CSCs and plays a role in promoting TKI resistance.
  • Targeting MAP17 or its associated pathways may offer a strategy to overcome TKI resistance in NSCLC.
Keywords:
MAP17cancer stem cellepidermal growth factor receptorresistancetyrosine kinase inhibitor

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