Ellagic acid inhibits gastric cancer cells by modulating oxidative stress and inducing apoptosis

Abstract

Objective: To evaluate the anticancer effect of ellagic acid on gastric cancer cells. Methods: MTT assay was used to evaluate the effect of ellagic acid at different concentrations (0.5-100 μg/mL) on gastric cancer AGS cells. RT-qPCR and Western blot analyses were applied to assess apoptosis (BCL-2, CASP-3, and BAX) and autophagy (LC3, ATG5, and BECN1) in AGS cells treated with ellagic acid. The expression of invasion-related markers including TP53, CDKN2A, and PTEN was determined. In addition, cell cycle markers including cyclin A, B, D, and E were measured by ELISA. Oxidative stress markers were evaluated using spectrophotometry. Results: Ellagic acid inhibited the proliferation of AGS cells in a concentration-and time-dependent manner. The expression of BCL-2 was significantly decreased (P<0.05) and CASP-3 and BAX were markedly increased (P<0.01) in AGS cells treated with ellagic acid. However, this compound induced no significant changes in the expression levels of LC3, ATG5, and BECN1 (P>0.05). Moreover, the oxidative stress markers including SOD, TAC, and MDA were increased by ellagic acid (P<0.01). Conclusions: Ellagic acid can inhibit cell proliferation, induce apoptosis, and modulate oxidative stress in AGS cells. However, further in vivo and molecular studies are needed to verify its anticancer efficacy.