RÉSUMÉ
Background and purpose:Studies have shown that DOC-2 could work as a potential tumor suppressor geue,and the role of DOC-2 in terms of the inhibition of cell growth and its mechanism remain unknown.Our paper is to investigate the effect and mechanism of DOC-2 expression on the tumorigenesis viability of ovarian cancer cell line HO-8910 from the aspects of clone efficiency,cell cycle and animal model test.Methods:Three cell lines were used including HO-8910,8910-P93(transfected with DOC-2 gene) and 8910-pcDNA3.1(transfected with the vector pcDNA3.1).Firstly,soft agar method was used to measure the clone efficiency.The cell cycle were analyzed by flow cytometer.The tumorigenesis viability was compared by athymic mouse test.Results:After being transfected with DOC-2 gene,the clone efficiency of 8910-P93 was markedly reduced.There was no difference between the 8910-pcDNA3.1 and HO-8910.G1 and G2 arrest were observed for 8910-P93.The athymic mouse test showed that the neoplasm derived from 8910-P93 was much smaller than that in the controls.Conclusions:DOC-2 could iniibit the tumorigenesis viability of human ovarian cancer line HO-8910.