Figures & data
Figure 1. Genistein inhibited the proliferation of HCT-116 (A) and LoVo (B) cells. Cells were treated with 0, 25, 50, and 100 μM of genistein for 24, 48, and 72 h. The cell viability was determined by the MTT assay. The results were presented as mean ± SD for triplicate experiments. *p < 0.05 versus each control group (0 µM).
Figure 2. Cell morphology under fluorescence microscopy by Hoechst 33258 staining in HCT-116 cells treated with genistein for 48 h. (A) Control group (0 μM). (B) Treated with genistein (25 μM). (C) Treated with genistein (50 μM). (D) Treated with genistein (100 μM). Arrows indicate the condensed and fragmented nuclei. The images were taken using an Olympus IX71FL fluorescence microscope (Olympus, Tokyo, Japan) (× 400).
Figure 3. Genistein decreased the expression of Bax in HCT-116 cells. (A) HCT-116 cells were treated with 0, 25, 50, and 100 μM of genistein for 48 h. The mRNA levels of Bax were determined by real-time PCR with GAPDH as internal control. (B) HCT-116 cells were treated with 0, 25, 50, and 100 μM of genistein for 48 h. The protein levels of Bax were determined by Western blot with β-actin as loading control. The results of real-time PCR and western blot assays are presented as mean ± SD for triplicate experiments. *p < 0.05 versus the control group (0 µM).
Figure 4. Treatment of HCT-116 cells with genistein resulted in reduced phosphorylation of Akt. HCT-116 cells were treated with 0, 25, 50, and 100 μM of genistein for 48 h. Total protein was extracted for immunoblotting of p-Akt and total Akt. The quantification of the western blot assays is presented as mean ± SD for triplicate experiments. *p < 0.05 versus the control group (0 µM).
