Abstract
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.
Highlights
Gastric cancer is a cancer which develops from the inner lining of the stomach
CARD exhibits a variety of biological activities such as anti-inflammatory and anti-tumor, so we hypothesize that CARD exerts anti-tumor activity by regulating cancer-related long non-coding RNA (LncRNA)-PVT1-signal transducer and activator of transcription 3 (STAT3) axis
Bcl-2 protein family determines the commitment of cells to trigger the mitochondrial suicide program apoptosis
Summary
Gastric cancer is a cancer which develops from the inner lining of the stomach. According to the World Health Organization (WHO), gastric cancer is the fifth most common cancer, but the third leading cause of cancer-related deaths each year all over the world [1]. Because the majority of people diagnosed with gastric cancer already at the advanced stage, patients often respond poorly to chemotherapy that causes long-term and serious side effects, resulting in a 5-year survival rate of less than 5%. 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. 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
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