The human umbilical cord MSCs were isolated and cultured. The morphology of cells were observed by light microscope. The expressions of surface antigen markers CD90， CD105， CD34 and CD45 were identified by flow cytometry. The MSCs were added with second antibody （without first antibody） were used as parallel control group.The conditioned medium containing 20% and 60% MSCs and cervical cancer HeLa cells were co-cultured for 72 h， colony formation experiment was used to observe the colony forming ability of HeLa cells after treated with of MSCs conditioned medium.CCK-8 experiment was used to detect the inhibitory rates of proliferation of the HeLa cells. Flow cytometry was used to detect the apoptotic rates of HeLa cells. Western blotting method was used to detect the expression levels of proliferation- and apoptosis-related gene proteins in the HeLa cellsn.

After 72 h of inoculation， a small number of cells adhered to the wall， and gradually became flat monolayer cells， which grew in clusters and vortices after one week. With the increase of cell density， the cell body became slender， similar to that of fibroblasts.The MSCs showed positive expressions of CD90 and CD105， but negative expressions of CD34 and CD45， which conformed to the phenotype of stem cells.The results of colony formation test showed that the inhibitory rates of colony formation of HeLa cells were 18.56% and 37.64% respectively when the conditioned medium containing 20% and 60% MSCs were added.Compared with control group，the early apoptotic rate of HeLa cells after treated with MSCs for 48 h was increased （P<0.05）. After the HeLa cells were treated with MSCs for 0， 24 and 48 h， the expression levels of cysteinyl aspartate-specific proteinase-3 （Caspase-3） and P53 proteins were increased continuously （P<0.05）， and the expression levels of B-cell lymphoma-2 （Bcl-2） protein were decreased continuously （P<0.05）.

The MSCs can inhibit the proliferation of HeLa cells and induce the apoptosis of HeLa cells in vitro，and its mechanism may be related to up-regulating the expression of Caspase-3 and P53 and down-regulating the expression of anti-apoptotic factor Bcl-2.