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miR-365a-5p suppresses gefitinib resistance in non-small-cell lung cancer through targeting PELI3

Fannian Li1, Haitao Li2, Shuai Li2

  • 1Department of Thoracic Surgery, The First Hospital of XingTai, No. 376 Shunde Road, XingTai, Hebei, 054001, China.

Pharmacogenomics
|July 9, 2020
PubMed

Insights

Dysregulated miR-365a-5p-PELI3 signaling drives gefitinib resistance in non-small-cell lung cancer (NSCLC). Restoring miR-365a-5p levels can overcome this resistance, offering a potential therapeutic strategy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Gefitinib is a crucial treatment for non-small-cell lung cancer (NSCLC) targeting EGFR.
  • Acquired resistance to gefitinib remains a significant clinical challenge in NSCLC treatment.
  • MicroRNAs (miRNAs) play a role in cancer development and drug resistance.

Purpose of the Study:

  • To investigate the role of the miR-365a-5p-PELI3 signaling axis in gefitinib resistance in NSCLC.
  • To elucidate the mechanism by which miR-365a-5p influences gefitinib sensitivity.
  • To explore the potential of targeting this axis for overcoming gefitinib resistance.

Main Methods:

  • Analysis of miR-365a-5p levels in NSCLC patients with varying gefitinib sensitivity.
  • In vitro experiments using NSCLC cell lines (PC9 and PC9GR) to study miR-365a-5p and PELI3 interactions.
  • In vivo studies using nude mice to assess the effect of miR-365a-5p on tumor growth.
  • Luciferase reporter assays to confirm direct targeting of PELI3 mRNA by miR-365a-5p.

Main Results:

  • Patients with primary resistance to gefitinib exhibited significantly lower levels of miR-365a-5p.
  • MiR-365a-5p was confirmed to directly target and regulate PELI3 mRNA expression.
  • Overexpression of miR-365a-5p enhanced the efficacy of gefitinib in inhibiting NSCLC cell viability.
  • Restoration of miR-365a-5p levels suppressed tumor growth in a preclinical mouse model.

Conclusions:

  • The dysregulated miR-365a-5p-PELI3 signaling axis is a key driver of gefitinib resistance in NSCLC.
  • Modulating miR-365a-5p levels holds promise for reversing gefitinib resistance.
  • Targeting the miR-365a-5p-PELI3 pathway represents a potential therapeutic strategy for improving gefitinib treatment outcomes in NSCLC.
Keywords:
PELI3gefitinib resistancemiR-365a-5pnon-small-cell lung cancer

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