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Updated: Apr 16, 2026

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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Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

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ANP32E drives lung adenocarcinoma progression via GSK3β-mediated glycolytic reprogramming

Zhongliang Wang1, Qianxia Li2, Zeguang Ye3

  • 1Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Cell Death & Disease
|April 14, 2026
PubMed

Insights

ANP32E drives lung adenocarcinoma (LUAD) progression by upregulating KDM3B and EGFR, impacting glycolysis and patient prognosis. The compound PGG effectively targets this pathway, offering a potential therapeutic strategy for LUAD.

Area of Science:

  • Oncology
  • Epigenetics
  • Metabolic Pathways

Background:

  • Lung adenocarcinoma (LUAD) is a major cause of cancer death.
  • The epigenetic-metabolic crosstalk in LUAD remains poorly understood.

Purpose of the Study:

  • Identify key regulators of LUAD progression.
  • Elucidate the molecular mechanisms driving LUAD.
  • Evaluate potential therapeutic targets and compounds.

Main Methods:

  • Multi-omics analysis (TCGA, scRNA-seq)
  • LUAD cell line experiments (proliferation, migration, glycolysis)
  • Xenograft models
  • Histone modification analysis
  • Signaling pathway investigation
  • High-throughput drug screening
  • Molecular dynamics simulations

Main Results:

  • ANP32E overexpression correlates with poor LUAD prognosis.
  • ANP32E promotes LUAD cell proliferation, migration, glycolysis, and tumor growth.
  • ANP32E upregulates KDM3B, reducing H3K9me2 at the EGFR promoter, enhancing EGFR transcription and activating PI3K/AKT/GSK3β signaling.
  • Penta-O-galloyl-β-D-glucose (PGG) inhibits the ANP32E/KDM3B/EGFR axis and suppresses LUAD growth.

Conclusions:

  • ANP32E is a key driver of LUAD progression through the KDM3B/EGFR/GSK3β axis.
  • ANP32E serves as a prognostic biomarker for LUAD.
  • PGG demonstrates therapeutic potential against LUAD by targeting the ANP32E pathway.

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