Taxifolin suppresses the malignant progression of gastric cancer by regulating the AhR/CYP1A1 signaling pathway

The development of novel approaches for the treatment of gastric cancer is of utmost importance. Taxifolin (Tax) has been reported to possess biological activities against a number of types of cancer. The objective of the present study was to examine the effects of Tax on gastric cancer and to explore its potential mechanisms of action. For this purpose, AGS and NCI-N87 cells, as well as BALB/c mice with gastric cancer cell-derived tumors were treated with Tax. Cell Counting Kit-8 and colony formation assays were performed to detect cell viability and proliferation, respectively. Wound-healing and Transwell assays were also conducted to determine the cell migratory and invasive abilities, respectively. Western blot analysis was performed to determine protein expression in vitro and in vivo. The results revealed that Tax significantly inhibited the viability, proliferation, migration and invasion of gastric cancer cells through the aryl hydrocarbon receptor (AhR)/cytochrome P450 1A1 (CYP1A1) signaling pathway. SB203580, an AhR agonist, partly abolished the inhibitory effects of Tax on gastric cancer cell viability, proliferation, migration and invasion. In addition, Tax also suppressed tumor growth in vivo. Collectively, the present study demonstrated that Tax significantly suppressed the tumor characteristics of gastric cancer. Tax may thus prove to be a potential therapeutic strategy for gastric cancer.