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Therapeutic potential of matrine and osthole against copper-promoted lung cancer cell malignancy

  • 0Henan International Collaborative Laboratory for Air Pollution Health Effects and Intervention, School of Public Health, Henan Medical University, Xinxiang, Henan Province 453003, China.
Pharmacotherapy +

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September 6, 2025

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September 6, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

Low-dose copper exposure promotes non-small cell lung cancer (NSCLC) cell growth and invasion. Natural compounds osthole and matrine reversed these effects by modulating key cellular pathways.

Area Of Science

  • Environmental toxicology
  • Cancer biology
  • Pharmacology

Background

  • Non-small cell lung cancer (NSCLC) is a leading cause of cancer mortality.
  • Environmental copper (Cu) exposure is increasingly recognized as a potential risk factor for NSCLC progression.

Purpose Of The Study

  • To investigate the impact of low-dose copper exposure on NSCLC A549 cells.
  • To evaluate the therapeutic potential of osthole and matrine against copper-induced NSCLC progression.

Main Methods

  • Exposure of A549 cells to low-dose copper (5 μg/mL, 12 h).
  • Treatment with natural compounds osthole and matrine.
  • Assessment of cell migration, invasion, apoptosis, ROS levels, mitochondrial potential, cell cycle, and gene/protein expression (qPCR, Western blot, TEM).

Main Results

  • Copper exposure significantly enhanced A549 cell migration, invasion, and colony formation, while reducing apoptosis and ROS levels.
  • Osthole and matrine treatments counteracted copper's pro-cancer effects, inducing G1 cell cycle arrest and causing mitochondrial damage.
  • Copper exposure altered the expression of PGC-1α, STAT1, TNF-α, and IL-2, with osthole and matrine differentially modulating these markers.

Conclusions

  • Low-dose copper exposure promotes NSCLC cell proliferation, migration, invasion, and mitochondrial dysfunction.
  • Osthole and matrine demonstrate therapeutic potential by inhibiting copper-induced NSCLC progression through regulation of STAT1, PGC-1α, TNF-α, and IL-2 pathways.

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