title: Apoptosis triggered by vitexin in U937 human leukemia cells via a mitochondrial             signaling pathway.
abstract: Vitexin, a lignan compound, has been shown to exert apoptotic actions on             human breast cancer cell lines and to have anti-inflammatory activities. Nevertheless,             there is currently no study addressing the effects of vitexin on the induction             of apoptosis in U937 human leukemia cells. The aim of this study was to determine             the anticancer effects and molecular mechanisms of vitexin on U937 leukemia cells.             We showed that vitexin can potently induce programmed cell death in U937 leukemia             cell growth as well as morphological changes that were examined by MTT assay and             phase contrast microscopy, respectively. The DNA content and the levels of mitochondrial             membrane potential (∆Ψm) were determined by flow cytometric analysis. The cell             cycle arrest-regulated and apoptosis-associated protein levels were measured by             western blotting. Vitexin-triggered apoptosis was accompanied by a decrease of             the level of ∆Ψm and the percentage of viability and provoked apoptosis in U937             cells. The downregulation of the protein level for Bcl-2 with the simultaneous             upregulation of caspase-3 and -9 protein expression in U937 cells were observed             after treatment with vitexin. Therefore, our data provide a potential mechanism             for the chemopreventive activity of vitexin, and we suggest that vitexin may serve             as a therapeutic agent for the treatment of human leukemia.
authors.affiliation: School of Pharmacy, China Medical University, Taichung, Taiwan, ROC.
authors.forename: Chao-Ying
authors.initials: CY
authors.lastname: Lee
authors.forename: Yung-Shin
authors.initials: YS
authors.lastname: Chien
authors.forename: Tai-Hui
authors.initials: TH
authors.lastname: Chiu
authors.forename: Wen-Wen
authors.initials: WW
authors.lastname: Huang
authors.forename: Chi-Cheng
authors.initials: CC
authors.lastname: Lu
authors.forename: Jo-Hua
authors.initials: JH
authors.lastname: Chiang
authors.forename: Jai-Sing
authors.initials: JS
authors.lastname: Yang
mesh_terms: D047310:Apigenin / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000378:metabolism; D053453:Caspase 9 / Q000378:metabolism; D059447:Cell Cycle Checkpoints / Q000187:drug effects; D004273:DNA, Neoplasm / Q000032:analysis; D015536:Down-Regulation; D006801:Humans; D007938:Leukemia / Q000378:metabolism* / Q000473:pathology*; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D015398:Signal Transduction / Q000187:drug effects*; D020298:U937 Cells; D015854:Up-Regulation
chemical_list: D004273:DNA, Neoplasm; D019253:Proto-Oncogene Proteins c-bcl-2; D047310:Apigenin; C032731:vitexin; D053148:Caspase 3; D053453:Caspase 9