[Effects of genistein on apoptosis in HCT-116 human colon cancer cells and its mechanism].

OBJECTIVE: To investigate the effects of genistein on cell proliferation and apoptosis in HCT-116 human colon cancer cells and its possible mechanism. METHODS: After treatment with genistein, cell proliferation was determined by MTT assay. Cell cycle, cell apoptosis, intracellular reactive oxygen species ( ROS) and mitochondrial membrane potential were determined by flow cytometry. Furthermore, ultrastructural change was observed using transmission electron microscopy (TEM). RESULTS: Genistein inhibited cell proliferation in a dose- and time-dependent manner. Genistein treatment in 0 - 100 micromol/L resulted in G2/M cell cycle arrest. The ratio of Sub-G1 increased from (1.63 +/- 0.44)% to (8.33 -1.51)% (P < 0.01). The ratio of early apoptosis increased from (1.93 +/- 0.32)% to (7.25 +/- 0.86)% (P < 0.01). Genistein caused characteristic apoptotic changes in TEM observation. Genistein treatment in 100 micromol/L increased intracellular ROS level to a peak at 2 h [2 h, (15.53 +/- 1.55)% vs. 0 h, (8.57 +/- 0.35)%, P < 0.01] and decreased mitochondrial membrane potential to a bottom at 1 h [1 h, (0.82 +/- 0.02)% vs. 0 h, (6.70 +/- 0.21)%, P < 0.01). CONCLUSION: Our findings indicated that genistein inhibits cell proliferation, induces G2/M cell cycle arrest and apoptosis in colon cancer cell line HCT-116, with the increase of intracellular ROS level and decrease of mitochondrial membrane potential.