Cardamonin exerts anti-gastric cancer activity via inhibiting LncRNA-PVT1-STAT3 axis.
Zheng WangXiaoli TangXiaoqing WuMeiyuan YangWei WangLiuhua WangDong TangDaorong WangPublished in: Bioscience reports (2019)
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.
Keyphrases
- cell proliferation
- cell cycle
- papillary thyroid
- induced apoptosis
- signaling pathway
- oxidative stress
- endoplasmic reticulum stress
- squamous cell
- poor prognosis
- long non coding rna
- gene expression
- dna methylation
- clinical evaluation
- long noncoding rna
- childhood cancer
- cell death
- squamous cell carcinoma
- immune response
- lymph node metastasis
- toll like receptor
- cell cycle arrest
- climate change