title: VI-16, a newly synthesized flavonoid, induces apoptosis through the             mitochondrial pathway in human hepatoma cells.
abstract: 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 bcl-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.
authors.affiliation: Jiangsu Key Laboratory of Carcinogenesis and Intervention, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing 210009, PR China.
authors.forename: Na
authors.initials: N
authors.lastname: Lu
authors.forename: Libin
authors.initials: L
authors.lastname: Wei
authors.forename: Dandan
authors.initials: D
authors.lastname: Gong
authors.forename: Yuan
authors.initials: Y
authors.lastname: Gao
authors.forename: Qinsheng
authors.initials: Q
authors.lastname: Dai
authors.forename: Zhiyu
authors.initials: Z
authors.lastname: Li
authors.forename: Qinglong
authors.initials: Q
authors.lastname: Guo
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects* / Q000235:genetics; D006528:Carcinoma, Hepatocellular / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D053148:Caspase 3 / Q000235:genetics; D053181:Caspase 8 / Q000235:genetics; D053453:Caspase 9 / Q000235:genetics; D061945:Caspase Inhibitors; D045744:Cell Line, Tumor; D005419:Flavonoids / Q000494:pharmacology*; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D016158:Genes, p53; D056945:Hep G2 Cells; D006801:Humans; D008113:Liver Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects / Q000235:genetics; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics; D015398:Signal Transduction / Q000187:drug effects; D051028:bcl-2-Associated X Protein / Q000235:genetics
chemical_list: D000970:Antineoplastic Agents; D061945:Caspase Inhibitors; D005419:Flavonoids; D019253:Proto-Oncogene Proteins c-bcl-2; C574191:VI-16 flavonoid; D051028:bcl-2-Associated X Protein; D053148:Caspase 3; D053181:Caspase 8; D053453:Caspase 9