Cardamonin exerts anti-gastric cancer activity via inhibiting LncRNA-PVT1-STAT3 axis

Background: Gastric cancer is one of the most commonly diagnosed cancers each year, and it remains the third leading cause of cancer death in the world. The clinicopathologic characteristics differ among regions, so epigenetic changes play a key role in gastric carcinogenesis. Methods: In the present study, we first demonstrate that cardamonin, a natural production of chalcone, is an anti-gastric cancer agent in pre-clinical evaluation. Results: Cardamonin inhibited proliferation and migration, induced apoptosis in gastric cancer cells. It could reduce the expression of apoptosis-related and migration-related genes and proteins. The constant activation of STAT3 (signal transducer and activator of transcription 3) signal is a major intrinsic signal for cancer inflammation. It regulates cellular proliferation, cell cycle, and migration that are critical for cancer procession. Cardamonin could effectively down-regulate p-STAT3 and abolish activation of STAT3 through inhibiting the expression of LncRNA-PVT1. Conclusion: The present study revealed that cardamonin is a potential natural source of anti-gastric cancer drugs via epigenetic mechanism to inhibit LncRNA-PVT1-STAT3 axis.