Study on the Mechanism of Arsenic Trioxide Complex Inhibiting the Growth of Human Glioma Cell Line U87

OBJECTIVE To study the effect of arsenic trioxide complex on the apoptosis of human glioma U87 cells and further explore its mechanism.METHODS Laser confocal method was used to study the way of arsenic trioxide complex entering cells. Cell scratch healing experiment was used to observe the effect on migration ability of U87 cells. Angiogenesis experiment was used to observe the ability of influencing neovascularization. Cell cycle and apoptosis were detected by flow cytometer. Immunoblotting method was used to detect the apoptosis related proteins of Bcl-2, Bax and caspase-3. RESULTS Arsenic trioxides mainly entered the cells by endocytosis, which could significantly inhibit the migration ability and neovascularization of U87 cells. Arsenic trioxides blocked the cell cycle of U87 cells at the G2/M phase, and promoted the early apoptosis of cells. Arsenic trioxides promoted the expression of Bax and caspase-3, and inhibited the expression of Bcl-2. CONCLUSION The inhibition mechanism of arsenic trioxide complex on U87 cells may be up-regulation of Bax expression and down-regulation of Bcl-2 expression after entering cells by endocytosis, leading to cell apoptosis.