Research Paper Volume 12, Issue 7 pp 6240—6259

Inhibition of esophageal-carcinoma cell proliferation by genistein via suppression of JAK1/2-STAT3 and AKT/MDM2/p53 signaling pathways

Figure 3. Genistein inhibits the expression of cell cycle-related genes and promotes the expression of cell apoptosis-associated genes. (A–C) The mRNA and protein levels of Bcl-2, Bcl-xl, Bax and Bid in Eca-109 cells treated with genistein for 72 h were determined through qPCR and western blotting. (D) The mRNA levels of PARP and Caspase-3 in Eca-109 cells treated with genistein for 72 h. (E, F) The protein levels of PARP, Caspase-3, cleaved PARP and cleaved Caspase-3 in Eca-109 cells treated with genistein for 72 h. (G–I) The mRNA and protein levels of P53, CyclinD1, CDK6 and CDK4 in Eca-109 cells treated with genistein for 72 h. (J) The mRNA and protein levels of Bax, Bid, Bcl-2, Bcl-xl, PARP, Caspase-3, CyclinD1, CDK4, CDK6 and P53 in xenograft tumor tissues were validated using qPCR and western blotting. Tumor-bearing nude mice were treated using different concentrations of genistein (5 mg/kg or 10 mg/kg) through gavage every 2 d (total time, 42 d; n = 6 per group). (K, L) Ki-67 expression in xenograft tumor tissues was tested through immunohistochemistry. Scale bar, 100 μm. All experiments were independently repeated in triplicate. Data are analyzed using one-way ANOVA with Dunnett’s test and presented as the mean ± SD. *P<0.05; **P<0.01; ***P<0.001; C-, cleaved.