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NOP58 modulates radiosensitivity in non-small cell lung cancer via DDX18-mediated DNA damage repair

Yiqian Jiang1, Weijun Zhang2, Yanhong Bao1

  • 1Department of Radiotherapy, Xiaoshan Affiliated Hospital of Wenzhou Medical University, No. 199, South Shixin Road, Xiaoshan District, Hangzhou City, Zhejiang, Province, 311200, China.

Journal of Radiation Research
|March 16, 2026
PubMed

Insights

Non-small cell lung cancer (NSCLC) is often resistant to radiation therapy. This study found that NOP58 promotes NSCLC radioresistance by interacting with DDX18, suppressing DNA damage, and suggests targeting the NOP58-DDX18 axis to improve treatment outcomes.

Area of Science:

  • Oncology
  • Molecular Biology
  • Radiotherapy Research

Background:

  • Non-small cell lung cancer (NSCLC) has poor survival rates, especially in advanced stages.
  • Radiation resistance significantly limits the effectiveness of radiotherapy for NSCLC.
  • The role of NOP58 in NSCLC radioresistance was previously unknown.

Purpose of the Study:

  • To investigate the underlying mechanisms of NOP58 in promoting radioresistance in NSCLC.
  • To explore the potential of targeting the NOP58-DDX18 interaction as a therapeutic strategy.

Main Methods:

  • Established a radiation-resistant NSCLC cell line (H1299R).
  • Utilized bioinformatics (TCGA), quantitative PCR, Western blot, cell viability assays (CCK-8, colony formation), apoptosis assays (flow cytometry), and DNA damage analysis (γ-H2AX, comet assay).
  • Performed gene knockdown (NOP58) and overexpression (DDX18) for rescue experiments and validated protein interactions via pull-down assays.

Main Results:

  • High NOP58 expression correlated with poor prognosis in NSCLC patients.
  • NOP58 and DDX18 were upregulated in radioresistant H1299R cells.
  • NOP58 depletion increased DNA damage and apoptosis, reversing radioresistance, while DDX18 overexpression counteracted these effects.
  • NOP58 directly interacts with DDX18, suppressing radiation-induced DNA damage and promoting cell survival.

Conclusions:

  • NOP58 promotes NSCLC radioresistance through its interaction with DDX18, which regulates gene expression and inhibits DNA damage.
  • The NOP58-DDX18 axis represents a potential therapeutic target for enhancing radiotherapy efficacy in NSCLC.
Keywords:
DNA damage repairNOP58 ribonucleoproteindead-box helicase 18non-small cell lung cancerradioresistance

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