Abstract: Objective To investigate the effects of neogambogic acid on proliferation and apoptosis of human breast cancer cell line MCF-7 and its mechanism. Methods MCF-7 cells were treated with different concentrations of neogambogic acid（0.5-20μg／ml） for 72 hours, and cell proliferation inhibition rate was detected by methyl thiazolyl tetrazolium（MTT） testing. Cell apoptosis was tested by flow cytometry（FCM） method with Annexin VFITC/PI double staining. Mitochondrial membrane potential changes were detected by JC-1 test. Expression levels of Fas, FasL， caspase-3, caspase-8, caspase9， Bax and Bcl-2 proteins were detected by Western blotting method. ResultsThe proliferation of MCF-7 cells were inhibited in a dosedependent manner when they were treated with 0.5-20 μg／ml neogambogic acid for 72h and IC50 was 1.763 μg／ml.0.5-3.0 μg／ml neogambogic acid could induce MCF-7 cells apoptosis in a dose and timedependent manner. Early apoptosis rate and total apoptosis rate of MCF-7 cells treated with 0.5μg／ml neogambogic acid for 48h were 3.7％ and 7.2％， and those were 6.7％ and 13.7％ for 72h. Early apoptosis rate and total apoptosis rate of MCF-7 cells treated with 3μg／ml neogambogic acid for 48h were 69.5％ and 71.7％， and those were 76.9％ and 81.5％ for 72h. Neogambogic acid（0.5, 1.0, 1.5 μg／ml） was effective to increase the proportion of mitochondrial transmembrane potential damaged cells. Apoptosis related protein FasL， caspase-3, caspase-8 and caspase-9 expression levels were increased in a dose-dependent manner. Fas and Bax protein levels changed little. The expression level of antiapoptotic protein Bcl-2 was decreased in a dosedependent manner. ConclusionNeogambogic acid can inhibit cell proliferation of human breast cancer cell line MCF-7 by inducing cell apoptosis， and the mechanism may relate to death receptor and mitochondrial pathway.