Fig. 10.

Apigenin administration inhibits 22Rv1 tumor growth in athymic nude mice via modulation of p53 signaling pathways. Approximately 1 million cells were injected into both flanks of each mouse to initiate ectopic prostate tumor growth, and apigenin was provided to the animals 2 weeks before cell inoculation. Mice were fed ad libitum with Teklad 8760 autoclaved high-protein diet. Apigenin was provided with 0.5% methyl cellulose and 0.025% Tween 20 as vehicle to these animals perorally on a daily basis. Group I, control, received 0.2 ml vehicle only, Group II received 20 μg apigenin per mouse in 0.2 ml vehicle, and Group III received 50 μg apigenin per mouse in 0.2 ml vehicle daily for 8 weeks. Once the tumor xenografts started growing, their sizes were measured twice weekly in two dimensions throughout the study. (A) Tumor volume (mm³) in control and treated groups. (B) Wet weight of tumors is represented as the mean of 8–10 tumors from each group. (C) Apoptosis as demonstrated by ELISA for 22Rv1 tumors after apigenin intake at the indicated doses. Values are means±SE, n=6–8, repeated twice with similar results. (D) Immunoblots for p53, Ser15-p53, cytochrome c, Bax, Bcl-2, and caspase-3 in tumor lysates after apigenin intake at the indicated doses. The blots were stripped and reprobed with anti-actin antibody to ensure equal protein loading. Significantly different from control: **p<0.001.