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IGF2BP3-mediated NTSR1 m6A methylation enhances irinotecan resistance and lung adenocarcinoma malignant progression

Hao Ding1, Xuan Zhu1, Yongquan Pan1

  • 1Department of Respiratory Disease, Affiliated People's Hospital of Jiangsu University, Zhenjiang, China.

American Journal of Respiratory Cell and Molecular Biology
|September 23, 2025
PubMed
Abstract

Insights

Neurotensin receptor 1 (NTSR1) promotes lung adenocarcinoma (LUAD) progression and Irinotecan resistance. Its stability is enhanced by IGF2BP3-mediated m6A methylation, suggesting a therapeutic target for LUAD treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Neurotensin receptor 1 (NTSR1) is implicated in cancer development, but its role in lung adenocarcinoma (LUAD) malignancy and Irinotecan resistance is unclear.
  • Understanding the molecular mechanisms of NTSR1 in LUAD is crucial for developing effective therapeutic strategies.

Purpose of the Study:

  • To investigate the role of NTSR1 in LUAD progression and Irinotecan resistance.
  • To elucidate the underlying molecular mechanisms, including the involvement of IGF2BP3 and m6A methylation.

Main Methods:

  • Bioinformatics analysis of NTSR1 expression and prognosis in LUAD.
  • Quantitative real-time polymerase chain reaction (RT-qPCR) and western blot (WB) for NTSR1 expression.
  • Cell proliferation, cell cycle, apoptosis, migration, and invasion assays.
  • Comet assay and γ-H2AX immunofluorescence for DNA damage.
  • MeRIP-qPCR for m6A methylation analysis.
  • RNA immunoprecipitation (RIP) and dual luciferase assays for protein-RNA interaction.
  • Immunohistochemistry (IHC) in mouse tumor models.

Main Results:

  • NTSR1 is upregulated in LUAD, correlating with poor patient survival.
  • NTSR1 knockdown inhibits LUAD cell proliferation, migration, and invasion, while enhancing apoptosis and Irinotecan sensitivity.
  • IGF2BP3 interacts with NTSR1, promoting its transcriptional stability via m6A methylation.
  • NTSR1 knockdown increases Irinotecan sensitivity and DNA damage in LUAD models.

Conclusions:

  • IGF2BP3-mediated m6A methylation of NTSR1 accelerates LUAD progression and Irinotecan resistance.
  • Targeting the IGF2BP3-NTSR1 pathway offers a potential therapeutic approach for LUAD.
Keywords:
IGF2BP3NTSR1irinotecanlung adenocarcinomam6A methylation

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