Abstract: 　Objective　To explore the effect and mechanism of Trichostatin A (TSA) on the cell proliferation and apoptosis of breast cancer MDA-MB-23.　Methods　MTT, plate cloning experiments, flow cytometry were used to detect the effect of TSA on cell biological functions. qPCR and Western blot were applied to detect the effect of TSA on proliferation, apoptosis and MAPK signaling pathway. Mechanisms were detect by JNK pathway inhibitor in treatment.　Results　TSA inhibited the proliferation and apoptosis of breast cancer MDA-MB-231 cells in a dose-dependent manner; TSA could block the cell cycle of breast cancer MDA-MB-231 cells in G1 phase. TSA could upregulate the expression of protein and mRNA on P21, caspase-3, Bax and p-JNK, and down-regulate the expression of protein and mRNA of cyclin D1, Cdk4 and Bcl-2. The inhibition of JNK pathway inhibited the expression of p-JNK and the total apoptosis rate of MDA-MB-231 cells. The expression of Caspase-3, Bax and Bcl-2 decreased.　Conclusions　TSA can induce the apoptosis of MDA-MB-231 cells, the mechanism of which is to regulate the expression of apoptotic protein and induce apoptosis through phosphorylation of JNK in MAPK signaling pathway.

Key words: TSA, 　Breast cancer, 　Cell proliferation and apoptosis, 　JNK signaling pathway