title: The mechanism of neogambogic acid-induced apoptosis in human MCF-7 cells.
abstract: Neogambogic acid (NGA), an active ingredient in garcinia, can inhibit the growth of some solid tumors and result in an anticancer effect. We hypothesize that NGA may be responsible for the inhibition of proliferation of human breast cancer cell line MCF-7 cells. To investigate its anticancer mechanism in vitro, MCF-7 cells were treated with various concentrations of NGA. Results of MTT (methyl thiazolyl tetrazolum) assay showed that treatment with NGA significantly reduced the proliferation of MCF-7 cells in a dose-dependent manner. NGA could increase the expression of the apoptosis-related proteins FasL, caspase-3, caspase-8, caspase-9, and Bax and decrease the expression of anti-apoptotic protein Bcl-2 accompanied by the mitochondrial transmembrane damage. The antiproliferative effect of NGA on MCF-7 cells is due to the G(0)/G(1) arrest, increased apoptosis and activation of Fas/FasL and cytochrome C pathway. These results provide an important insight into the cellular and molecular mechanisms through which NGA impairs the proliferation of breast cancer cells.
authors.affiliation: The First Clinical Medicine School, Nanjing University of Chinese Medicine (NUCM), China.
authors.forename: Keming
authors.initials: K
authors.lastname: Wang
authors.forename: Yuhong
authors.initials: Y
authors.lastname: Tang
authors.forename: Ming
authors.initials: M
authors.lastname: Sun
authors.forename: Binbin
authors.initials: B
authors.lastname: Lu
authors.forename: Hongqin
authors.initials: H
authors.lastname: Zhu
authors.forename: Ou
authors.initials: O
authors.lastname: Ji
authors.forename: Qun
authors.initials: Q
authors.lastname: Shen
mesh_terms: D000972:Antineoplastic Agents, Phytogenic / Q000737:chemistry / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D015153:Blotting, Western; D001943:Breast Neoplasms / Q000378:metabolism / Q000473:pathology; D053148:Caspase 3 / Q000378:metabolism; D053181:Caspase 8 / Q000378:metabolism; D053453:Caspase 9 / Q000378:metabolism; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D045304:Cytochromes c / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D053222:Fas Ligand Protein / Q000378:metabolism; D005260:Female; D016193:G1 Phase / Q000187:drug effects; D029760:Garcinia / Q000737:chemistry; D006801:Humans; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D015394:Molecular Structure; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D016192:Resting Phase, Cell Cycle / Q000187:drug effects; D013729:Terpenes / Q000737:chemistry / Q000494:pharmacology*; D014966:Xanthenes; D044004:Xanthones / Q000737:chemistry / Q000494:pharmacology*; D051028:bcl-2-Associated X Protein / Q000378:metabolism; D019014:fas Receptor / Q000378:metabolism
chemical_list: D000972:Antineoplastic Agents, Phytogenic; C491901:FAS protein, human; D053222:Fas Ligand Protein; D019253:Proto-Oncogene Proteins c-bcl-2; D013729:Terpenes; D014966:Xanthenes; D044004:Xanthones; D051028:bcl-2-Associated X Protein; D019014:fas Receptor; D045304:Cytochromes c; C045863:neo-gambogic acid; D053148:Caspase 3; D053181:Caspase 8; D053453:Caspase 9