Abstract: Objective 　To study the effects of the OPCML in ovarian cancer cell lines. Methods 　The OPCML was t ransferred to the human ovarian cancer cell lines A2780 and OCC1 in addition to normal CD1 mouse ovarian surface epithelial cells by recombinant lentiviruses which carrying OPCML, the infected cells were then characterized by cell proliferation assays, cell aggregation assays, cell cycle analysis by flow cytometry( FCM) and tumorigenicity assays following injection into nude mice. Results 　(1) The efficiency of infection of the cell lines using the lentiviral vectors was almost 100 % allowing the stable expression of OPCML in nearly all cells. Stable expression of OPCML (60kDa) and GFP(27kDa) proteins was confirmed by Western blot analysis. (2) A2780 cells expressing OPCML grew slowly compared to A2780 parental or control virus infected cells ( P < 0. 01), but the expression of OPCML had no effect on the proliferation rates of OCC1 and the normal CD1 cells when compared to their respective parental or controls ( P > 0. 05) . (3) Flow cytometry based cell cycle assays showed that the expression of OPCML can arrest A2780 cells ( P < 0. 05) ; but not in OCC1, CD1 cells. (4) Cell aggregation assays indicated the OPCML can increase cell surface adhesion mediated. (5) A2780 cells expressing OPCML only formed a single tumor in mice and which was significantly smaller than cont rols (4/ 4) ( P < 0. 001) . Expression of OPCML in tumor was confirmed by immunohistochemisty. Conclusion 　The use of lentiviral vectors allowed the efficient expression of OPCML in nearly 100 % of target cells. Expression of the OPCML resulted in an increase of cell adhesion in all cell lines tested, and decreased the proliferation and tumorigenicity of the A2780 ovarian cancer cell line. It suggest s that the OPCML maybe a new tumor suppressor gene.