VI-16, a newly synthesized flavonoid, induces apoptosis through the mitochondrial pathway in human hepatoma cells

作者：Lu, Na; Wei, Libin; Gong, Dandan; Gao, Yuan; Dai, Qinsheng; Li, Zhiyu; Guo, Qinglong^*

来源：Oncology Reports, 2012, 27(3): 873-879.

DOI：10.3892/or.2011.1594

• apoptosis
• mitochondrial pathway
• p53
• VI-16
• anticancer

VI-16, a newly synthesized flavonoid, has a hydroxy substitution at C5 position, a methoxyl substitution at C5 position, and a piperazine substitution at C7 position. Here, we firstly investigated the potential antitumor effect of VI-16 in HepG2 human hepatocarcinoma cells. The MTT assay showed that VI-16 inhibited HepG2 cell growth in a concentration- and time-dependent manner. To further investigate whether apoptosis induction contributed to the antitumor effects of VI-16, DAPI staining and Annexin-V/PI double staining were performed in our tests. The data showed that VI-16 could induce apoptotic cell death in HepG2 cells. Moreover, mechanistic studies revealed that VI-16-induced apoptosis was a caspase-dependent process by decreasing the expression of pro-caspase-3. The changes in the expression of caspase-8, capsase-9, Bax and BcI-2 after VI-16 treatment suggested that the mitochondrial pathway was involved in the apoptosis induced by VI-16. Furthermore, VI-16 could significantly increase the loss of mitochondrial membrane potential and the expression of p53. Taken together, these results demonstrated that apoptosis induced by VI-16 might be one of the mechanisms by which VI-16 acts as a preventive antitumor drug against human hepatoma.

• 出版日期2012-3
• 单位中国药科大学