Fig. 5

Modulation of apoptosis in oral cancer cells by limocitrin through MAPK pathways. (A) Western blot assessment of phosphorylated AKT, ERK1/2, p38, and JNK1/2, with β-actin as the internal control. (B) Expression levels displayed as mean ± standard deviation (n = 3). *p < 0.05, indicating statistical significance compared with the control group. (C, D) Oral cancer cells were pretreated with the AKT inhibitor, LY294002, for 1 h and then treated with limocitrin for 24 h. Quantitation of cleaved caspase-3 and caspase-8 is illustrated. (E, F) Oral cancer cells were pretreated with the ERK inhibitor, U0126, for 1 h and then treated with limocitrin for 24 h. Quantitation of cleaved caspase-3 and caspase-8 is illustrated. All data are displayed as mean ± standard deviation (n = 3). *p < 0.05, indicating statistical significance compared with the control group. #p < 0.05, indicating statistical significance compared with limocitrin treatment alone.