Polydatin suppresses proliferation and metastasis of non-small cell lung cancer cells by inhibiting NLRP3 inflammasome activation via NF-kappa B pathway

Non-small cell lung cancer (NSCLC) is the leading cause of cancer death. Particularly, inflammation is crucial for the progression of NSCLC. In the past few decades, the anti-tumor effects of some traditional Chinese medicinal herbs have caused much attention. This study was designed to investigate the effects of polydatin in the progression of NSCLC. CCK-8 assay, wound healing assay and western blot assay were used to assess the anti-cancer property. Consequently, we showed that polydatin inhibited proliferation and migration of NSCLC cells (A549 and H1299 cells) in a dose-dependent manner. In addition, polydatin suppressed the expression of NLRP3, ASC and pro-caspase-1in NSCLC cells. Activation of NLRP3 inflammasome counteracted the inhibitory effect of polydatin on proliferation and migration of NSCLC cells, suggesting that polydatin suppressed progression of NSCLC through inhibiting NLRP3 inflammasome activation. Furthermore, polydatin was found to down-regulate relative expression of phosphor-NF-kappa B p65 and activation of NF-kappa B pathway by TNF-alpha also abolished the inhibitory effect of polydatin on proliferation and migration of NSCLC cells. In conclusion, our data showed that polydatin acted as an anti-tumor agent to suppress proliferation and metastasis of NSCLC cells. The anti-tumor effect of polydatin was possibly related to the inhibition of NLRP3 inflammation via the NF-kappa B pathway. Our finding suggested that polydatin might be a potential therapeutic candidate in the treatment of NSCLC.