Amygdalin suppresses the proliferation, migration and EMT of gastric cancer cells by inhibiting TGF-β/Smad signal pathway

Purpose: To investigate the effects of amygdalin on the proliferation, motility and epithelial mesenchymal transformation (EMT) of gastric cancer cells and to elucidate the operating mechanisms of action. Methods: Gastric cancer AGS cells were treated with amygdalin (2.5, 5 and 10 mg/L). MTT and colony formation assays were used to investigate the effect of amygdalin on gastric cancer cell proliferation, while wound healing and Transwell assays were also carried out to determine its effect on the motility of gastric cancer cells. Immunoblot assays were used to investigate the effects of amygdalin on epithelial mesenchymal transformation (EMT) process and TGF-beta/Smad pathway in gastric cancer cells. Results: Treatment with amygdalin suppressed the proliferation of gastric cancer AGS cells (p < 0.05). Amygdalin suppressed the migration and invasion of AGS cells in vitro (p < 0.05). Additionally, amygdalin suppressed epithelial mesenchymal transformation (EMT) in AGS cells, and suppressed TGF-beta/Smad pathway (p < 0.05), thereby suppressing growth, motility, and EMT in AGS cells. Conclusion: Amygdalin may be useful for the treatment of gastric cancer; however, further studies are required ascertain this.