Objective      To determine the effect of dichloroacetate (DCA) on the proliferation and apoptosis of cervical cancer cells

and investigate the possible mechanism.       Methods      CCK-8 assay was used to measure the effect of DCA on the proliferation of cervical cancer HeLa cells

and flow cytometry to detect its effect on cell apoptosis. Expression levels of apoptosis-associated proteins poly ADP-ribose polymerase (PARP) and myeloid cell leukemia-1 (Mcl-1) was measured in HeLa cells after DCA treatment by Western blot analysis.       Results      DCA treatment significantly suppressed the proliferation (P0.01)

enhanced the apoptosis (P0.01)

increased the level of cleaved PARP

and reduced the level of Mcl-1 protein in HeLa cells. Moreover

the DCA-mediated down-regulation of Mcl-1 protein in HeLa cells could be attenuated by proteasome inhibitor MG132

but not by translation inhibitor cycloheximide (CHX).       Conclusion      DCA promotes the apoptosis of cervical cancer HeLa cells

which may be resulted from the down-regulation of Mcl-1 protein by DCA-induced proteasomal degradation.