To investigate the influence of resveratrol (Res) on the growth of gastric cancer cells (AGS) in vitro and the underlying mechanism.

AGS cells were cultured with Res at different concentrations (25, 50, and 100 μmol/L) for 24, 48, or 72 h. MTT assay was used to determine the reduced growth of AGS cells at 24, 48, or 72 h after treatment. Flow cytometry was used to detect the cell cycle arrest at 24 h. Immunocytochemistry was used to detect the expression of Wnt1, beta-catenin, and Lgr5 at 24 h.

After AGS cells were treated with different concentrations of Res (25, 50, and 100 μmol/L) for different durations, the cells became round in morphology, decreased in density, and showed poorer adherence. Res inhibited cell proliferation in a time and dose dependent manner (25 μmol/L: 0.2033 ± 0.0207 at 24 h, 0.3949 ± 0.0199 at 48 h, 0.5102 ± 0.0155 at 72 h; 50 μmol/L: 0.3554 ± 0.0207 at 24 h, 0.5157 ± 0.0321 at 48 h, 0.6167 ± 0.0248 at 72 h; 100 μmol/L: 0.5005 ± 0.0199 at 24 h, 0.6251 ± 0.0299 at 48 h, 0.7271 ± 0.0147 at 72 h; P<0.05). Res arrested cells in G₁ phase in a concentration dependent manner (percentage of G₁ phase cells in control cells: 48.33 ± 0.21; 25 μmol/L: 52.61 ± 0.41; 50 μmol/L: 58.53 ± 0.48; 100 μmol/L: 71.16 ± 0.20, P<0.05). Res altered the expression of Wnt1 (100 μmol/L: 207.36 ± 0.52; 50 μmol/L: 202.65 ± 0.53; 25 μmol/L: 197.13 ± 1.07; control: 191.40 ± 0.28; P<0.05), beta-catenin (100 μmol/L: 206.51 ± 0.68; 50 μmol/L: 200.49 ± 0.30; 25 μmol/L: 196.53 ± 0.59; control: 191.98 ± 0.30; P<0.05), and Lgr5 (100 μmol/L: 209.22 ± 0.51; 50 μmol/L: 204.53 ± 0.92; 25 μmol/L: 195.7 ± 60.90; control: 188.16 ± 0.86; P<0.05) in a concentration dependent manner.

Res inhibits the growth of AGS cells probably by regulating the Wnt/beta-catenin signaling pathway.