The objective of this study was to examine the cytotoxic effects of farrerol on esophageal cancer cells. Firstly, the influence of farrerol on the vitality of esophageal cancer cells (EC109) was examined, revealing a significant detrimental effect on cellular viability. Subsequently, a flow cytometry examination was conducted to examine its role in the apoptotic process and cell cycle of EC109 cells. Farrerol has been found to effectively induce apoptosis and arrest the cell cycle at the G2/M phase. In addition, it leads to the activation of caspase-9, an increase in NADPH oxidase activity, and the formation of reactive oxygen species, while simultaneously reducing the level of glutathione in EC109 cells. Furthermore, a model of athymic nude mice was created by injecting EC109 cells to examine the pharmacological efficacy of farrerol. The results indicated that farrerol significantly decreases the size of the tumor and enhances the body weight of the mice. The western blot examination demonstrated that it suppressed the activity of phosphorylated epidermal growth factor receptor (p-EGFR) and phospho-transducer and activator of transcriptor-3 (p-STAT3) in the mice. The results of our study effectively showcased the pharmacological advantages of farrerol in treating esophageal cancer, owing to its multifactorial impact.
