Abstract
Previous studies have shown that various active components of licorice have anticancer effects. However, few studies have investigated the mechanism of action of licorice in gastric cancer. The effect of active compounds in licorice on the biological activity of gastric cancer cells was investigated in vitro (MKN-45 cells). Network pharmacology and molecular docking were used to predict the potential targets of licorice against gastric cancer and verify the binding stability of target proteins to compounds. In addition, the anticancer effect of licorice was assessed using a mouse model of gastric cancer. The licorice-active component (quercetin) effectively inhibited proliferation, caused cell cycle arrest, and promoted apoptosis in MKN-45 cells, accompanied by increased Cyt-C, decreased BCL-2, and decreased mitochondrial membrane potential and mitochondrial damage. Further research showed that quercetin targeted EGFR, blocked the ERK signaling pathway, and downregulated PTGS2. In the in vivo experiment, quercetin treatment resulted in reduced tumor volume, decreased Ki67 and BCL-2 expression in tumor tissue, increased caspase 3 and BAX levels, and induced mitochondrial damage.
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