Lung Cancer
Evidence-based overview of polydatin in lung cancer, including apoptosis, cell-cycle arrest, and cisplatin-synergy findings
Polydatin has strong preclinical relevance in lung cancer, especially in non-small-cell lung cancer models.
Overview
The lung cancer literature centres on apoptosis, S-phase arrest, and synergy with cisplatin.
Key findings
Inhibits proliferation of A549 and NCI-H1975 lung cancer cells in a dose-dependent manner
Causes apoptosis and S-phase cell-cycle arrest
Increases Bax and decreases Bcl-2
Suppresses cyclin D1 expression
Acts as a potential NOX5 agonist in NSCLC, enhancing cisplatin antitumour activity
Practical interpretation
The lung cancer evidence is still preclinical, but consistently supports polydatin as a redox-active and apoptosis-promoting adjunct.
References
Polydatin inhibits growth of lung cancer cells by inducing apoptosis and cell cycle arrest
https://pmc.ncbi.nlm.nih.gov/articles/PMC3861602/
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