title: Magnolol induces apoptosis in MCF-7 human breast cancer cells through G2/M phase arrest and caspase-independent pathway.
abstract: Magnolol, a small-molecule hydroxylated biphenol, isolated from the root and stem bark of Magnolia officinalis, has been shown to possess antiproliferative effect on various cancer cell lines. In the current study, we found that magnolol potently inhibited proliferation and induced apoptosis in MCF-7 human breast cancer cells. Further mechanistic studies revealed that induction of apoptosis is associated with cell cycle arrest at G2/M phase, increased generation of reactive oxygen species (ROS), reduced mitochondrial membrane potential (MMP), release of cytochrome c (Cyto c) and apoptosis inducing factor (AIF) from mitochondria to cytosol, upregulation of Bax, p21 and p53, and down-regulation of Bcl-2, cyclin B1 and cyclin-dependent kinase 1 (CDK1). Our findings indicated that magnolol induced apoptosis in MCF-7 cells via the intrinsic pathway with release of AIF from mitochondrial and G2/M phase arrest pathway. Therefore, magnolol might be a potential lead compound in the therapy of breast cancer.
authors.affiliation: School of Life Sciences, Liaoning Provincial Key Laboratory of Biotechnology and Drug Discovery, Liaoning Normal University, Dalian, China.
authors.forename: Yongfeng
authors.initials: Y
authors.lastname: Zhou
authors.forename: Yanying
authors.initials: Y
authors.lastname: Bi
authors.forename: Chunhui
authors.initials: C
authors.lastname: Yang
authors.forename: Jingbo
authors.initials: J
authors.lastname: Yang
authors.forename: Yu
authors.initials: Y
authors.lastname: Jiang
authors.forename: Fanmin
authors.initials: F
authors.lastname: Meng
authors.forename: Bo
authors.initials: B
authors.lastname: Yu
authors.forename: Muhammad
authors.initials: M
authors.lastname: Khan
authors.forename: Tonghui
authors.initials: T
authors.lastname: Ma
authors.forename: Hong
authors.initials: H
authors.lastname: Yang
mesh_terms: D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D051033:Apoptosis Inducing Factor / Q000378:metabolism; D001713:Biphenyl Compounds / Q000494:pharmacology*; D006690:Bisbenzimidazole; D001943:Breast Neoplasms / Q000188:drug therapy*; D020169:Caspases / Q000502:physiology*; D002455:Cell Division / Q000187:drug effects*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D004396:Coloring Agents; D045304:Cytochromes c / Q000378:metabolism; D005260:Female; D005434:Flow Cytometry; D016195:G2 Phase / Q000187:drug effects*; D019254:Genes, bcl-2 / Q000187:drug effects; D006801:Humans; D007202:Indicators and Reagents; D017705:Lignans / Q000494:pharmacology*; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D013778:Tetrazolium Salts; D013844:Thiazoles
chemical_list: D000972:Antineoplastic Agents, Phytogenic; D051033:Apoptosis Inducing Factor; D001713:Biphenyl Compounds; D004396:Coloring Agents; D007202:Indicators and Reagents; D017705:Lignans; D017382:Reactive Oxygen Species; D013778:Tetrazolium Salts; D013844:Thiazoles; C005498:magnolol; D045304:Cytochromes c; D020169:Caspases; C022616:thiazolyl blue; D006690:Bisbenzimidazole