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Wogonin Suppresses Non-Small Cell Lung Cancer Growth in Association with Oxidative Stress, c-Myc/GPX4 Downregulation

Hairong Xiang1, Haoshu Liu1, Ruyu Jiang1

  • 1College of Basic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, China.

Antioxidants (Basel, Switzerland)
|July 28, 2026
PubMed

Insights

Wogonin (WGN) combats non-small cell lung cancer (NSCLC) by increasing reactive oxygen species (ROS), inducing ferroptosis, and triggering apoptosis. This flavonoid targets key proteins, offering a potential therapeutic strategy for NSCLC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Antioxidant defense regulated by reactive oxygen species (ROS) is crucial in non-small cell lung cancer (NSCLC) progression and treatment resistance.
  • Wogonin (WGN), a flavonoid, exhibits antitumor properties, but its role in ROS-dependent ferroptosis and mitochondrial stress in NSCLC requires further investigation.

Purpose of the Study:

  • To elucidate the association between Wogonin (WGN) and ROS-dependent ferroptotic and mitochondrial stress in non-small cell lung cancer (NSCLC).
  • To investigate the molecular mechanisms underlying WGN's effects on NSCLC cell lines, xenografts, and patient-derived organoids.

Main Methods:

  • Utilized NSCLC cell lines (A549, BEAS-2B), mouse xenografts, patient-derived organoids, and transcriptomic data.
  • Assessed cell viability, colony formation, migration, invasion, ROS levels, mitochondrial potential, apoptosis, iron, and lipid peroxidation.
  • Employed RT-qPCR, Western blotting, immunofluorescence, and c-Myc gain/loss-of-function assays.

Main Results:

  • WGN inhibited A549 cell growth and motility, increasing intracellular ROS, iron (Fe2+), and lipid peroxidation.
  • WGN decreased mitochondrial membrane potential, induced apoptosis, and downregulated c-Myc, GPX4, and SLC7A11 while upregulating ACSL4.
  • Inhibitor rescue experiments and c-Myc manipulation confirmed WGN's impact on ferroptosis and apoptosis pathways.

Conclusions:

  • Wogonin (WGN) suppresses NSCLC phenotypes, particularly in A549 cells, through ROS accumulation, ferroptosis induction, and mitochondrial dysfunction-associated apoptosis.
  • The observed effects are linked to the downregulation of the c-Myc/GPX4 axis, highlighting a novel therapeutic mechanism for WGN in NSCLC.
Keywords:
Wogoninantioxidant defensec-Myc/GPX4ferroptosismitochondrial apoptosisnon-small cell lung canceroxidative stressreactive oxygen species

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