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Updated: Jul 14, 2025

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
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JMJD5 inhibits lung cancer progression by facilitating EGFR proteasomal degradation

Jing Shen1, Guiling Liu2, Hongyan Qi3

  • 1Department of Pathology and Pathophysiology, and Department of Medical Oncology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310058, China. shenjingwzy@zju.edu.cn.

Cell Death & Disease
|October 9, 2023
PubMed

Insights

Reduced JMJD5 expression promotes non-small cell lung cancer (NSCLC) growth. JMJD5 destabilizes epidermal growth factor receptor (EGFR), inhibiting NSCLC progression and overcoming TKI resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Aberrant epidermal growth factor receptor (EGFR) signaling drives non-small cell lung cancer (NSCLC) development.
  • EGFR tyrosine kinase inhibitors (TKIs) are challenged by resistance mutations.

Purpose of the Study:

  • Investigate the role of JmjC domain-containing 5 (JMJD5) in NSCLC.
  • Determine JMJD5's mechanism in regulating EGFR stability and TKI resistance.

Main Methods:

  • Assessed JMJD5 expression in relation to EGFR stability and NSCLC progression.
  • Elucidated JMJD5's interaction with E3 ligase HUWE1 for EGFR proteasomal degradation.
  • Investigated JMJD5's intercellular transport via extracellular vesicles.

Main Results:

  • Reduced JMJD5 expression correlates with increased EGFR stability and NSCLC progression.
  • JMJD5 destabilizes wild-type EGFR and TKI-resistant mutants via HUWE1 and proteasomal degradation.
  • Extracellular vesicle-mediated transport of JMJD5 inhibits NSCLC growth.

Conclusions:

  • JMJD5 acts as a tumor suppressor in NSCLC by destabilizing EGFR.
  • Targeting JMJD5 to degrade EGFR presents a potential therapeutic strategy for EGFR-mutated NSCLC and TKI resistance.

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