Objective To observe the effects of dichloroacetate (DCA)on the proliferation and apoptosis of bladder cancer cells T24 in vitro and to study the underlying mechanism. Methods The bladder cancer cells T24 were randomly divided into four groups: experimental group 1, experimental group 2, experimental group 3, and the control group. Cells in the experimental groups 1, 2, and 3 were added with 5, 10, and 20 mmol/ L DCA, respectively; cells in the control group were added with 0. 1% dimethyl sulfoxide (DMSO). The cell proliferation of T24 cells were detected by MTT assay at 24, 48, and 72 h after DCA treatment. At 48 h, the apoptosis was examined by Hoechst33258 staining,the mitochon-drial membrane potential was detected by using JC-1 staining,and the expression levels of Bax protein, Bcl-2 protein and Caspase-3 protein were determined by Western blotting. Results The cell proliferation in the experimental groups 1, 2, and 3 was lower than that of the the control group at 24, 48 and 72 h, and with the time and increasing concentrations of DCA, the inhibition of cell proliferation was more significant (all P < 0. 05). The number of apoptosis cells in the experimental groups 1,2 and 3 was higher than that of the control group, and the mitochondrial membrane potential was lower than that of the control group (all P < 0. 05). Compared with the control group, the expression of Bax protein and Caspase-3 protein significantly increased, while the expression of Bcl-2 protein significantly decreased in the experimental groups 1, 2, and 3 (all P < 0. 05). Conclusions DCA can inhibit the proliferation and induce the apoptosis of bladder cancer cell line T24, which suggests that the mechanism may be related to the decrease of mitochondrial membrane potential level,up-regulation of Bax protein and Caspase-3 protein, and down-regulation of Bcl-2 protein. [ABSTRACT FROM AUTHOR]