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Long Noncoding RNA LINC01116 Contributes to Gefitinib Resistance in Non-small Cell Lung Cancer through Regulating

He Wang1, Binbin Lu2, Shengnan Ren1

  • 1Department of Oncology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing 210011, People's Republic of China; Department of Oncology, Sir Run Run Hospital, Nanjing Medical University, Nanjing 211166, People's Republic of China.

Molecular Therapy. Nucleic Acids
|December 17, 2019
PubMed

Insights

Long non-coding RNA LINC01116 promotes gefitinib resistance in non-small cell lung cancer (NSCLC) by upregulating IFI44. Downregulating LINC01116 may overcome resistance to epidermal growth factor receptor tyrosine kinase inhibitors (TKIs) in NSCLC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are first-line treatments for non-small cell lung cancer (NSCLC).
  • Acquired resistance to TKIs like gefitinib poses a significant challenge to long-term patient survival and treatment efficacy.
  • Understanding the molecular mechanisms underlying TKI resistance is crucial for developing effective therapeutic strategies.

Purpose of the Study:

  • To investigate the role of the long non-coding RNA (lncRNA) LINC01116 in gefitinib resistance in NSCLC.
  • To elucidate the underlying molecular mechanism by which LINC01116 influences gefitinib sensitivity.
  • To explore LINC01116 as a potential therapeutic target for overcoming TKI resistance.

Main Methods:

  • Analysis of LINC01116 expression in gefitinib-resistant NSCLC cells and tissues.
  • Loss- and gain-of-function assays to assess the impact of LINC01116 on gefitinib resistance.
  • Investigation of the relationship between LINC01116 and IFI44 expression.
  • In vivo studies to evaluate the effect of LINC01116 downregulation on gefitinib sensitivity.

Main Results:

  • LINC01116 was found to be upregulated in gefitinib-resistant NSCLC cells and tissues.
  • Downregulation of LINC01116 sensitized NSCLC cells to gefitinib, while its overexpression conferred resistance.
  • LINC01116 silencing increased IFI44 expression, and IFI44 overexpression reversed gefitinib resistance.
  • LINC01116 affects gefitinib resistance partly through regulating IFI44 expression.
  • Downregulation of LINC01116 enhanced gefitinib sensitivity in vivo.

Conclusions:

  • LINC01116 plays a critical role in mediating gefitinib resistance in NSCLC.
  • The mechanism involves LINC01116 regulating IFI44 expression, thereby influencing TKI sensitivity.
  • LINC01116 represents a potential novel therapeutic target for overcoming TKI resistance in NSCLC patients.
Keywords:
IFI44LINC01116NSCLCTKI resistancegefitinib

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