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.