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Related Experiment Video

Updated: Jun 14, 2025

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Role of GNL3L in lung cancer: Mediating proliferation and progression through NF-κB pathway activation and

Qian Wang1, Xiao-Qi Zhang2, Shan-Shan Liu3

  • 1Department of Respiratory Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Hospital of Chinese Medicine, Nanjing, Jiangsu, 210029, China; Department of Respiratory Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Suqian Hospital of Chinese Medicine, Suqian, China.

Experimental Cell Research
|June 4, 2025
PubMed
Summary

Guanine Nucleotide-Binding Protein-Like 3-Like Protein (GNL3L) promotes lung cancer growth and spread by activating NF-κB and increasing Slug, MMP2, and MMP9. Inhibiting GNL3L may offer a new therapeutic strategy for non-small cell lung cancer.

Keywords:
BiomarkerGNL3LNF-κBNon-small cell lung cancerSlug

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • The role of Guanine Nucleotide-Binding Protein-Like 3-Like Protein (GNL3L) in lung cancer progression is not fully understood.
  • Lung adenocarcinoma (LUAD) is a major subtype of non-small cell lung cancer (NSCLC).

Purpose of the Study:

  • To investigate the impact of GNL3L on LUAD cell proliferation, migration, and invasion.
  • To elucidate the underlying molecular mechanisms.
  • To evaluate GNL3L as a potential therapeutic target.

Main Methods:

  • Inhibition of GNL3L expression in A549 and H1299 NSCLC cell lines.
  • In vivo tumor xenograft models in nude mice.
  • Analysis of NF-κB activation, Slug, MMP2, and MMP9 expression.
  • Rescue experiments involving Slug overexpression, NF-κB activation, and MMP2/MMP9 overexpression.

Main Results:

  • GNL3L inhibition significantly reduced proliferation, migration, and invasion of NSCLC cells in vitro.
  • GNL3L silencing decreased tumor volume and improved outcomes in vivo.
  • GNL3L suppression markedly inhibited NF-κB activation and reduced Slug, MMP2, and MMP9 expression.
  • Slug, NF-κB, MMP2, and MMP9 were identified as key mediators of GNL3L's pro-tumorigenic effects.

Conclusions:

  • GNL3L promotes lung cancer proliferation, migration, and invasion by activating the NF-κB pathway and upregulating Slug, MMP2, and MMP9.
  • Targeting GNL3L presents a promising therapeutic strategy for NSCLC, particularly in cases with GNL3L overexpression.