Objective    To explore the role of adaptor protein CrkⅠ in malignant potential of human ovarian cancer.     Methods    Crk and Dock180 expression were detected by Western blotting in ovarian cancer tissues (EOC

n=28)

benign ovarian tumors (BOT

n=13) and normal ovary tissues (Normal

n=10). Co-precipitation was performed to evaluate the in vivo protein-protein interaction of Dock180 and Crk in 3 different ovarian cancer cell lines (SKOV3

MCAS and RMUG-L cells). The expression of Crk in SKOV3 cells were silenced by using siRNA interference

and then Rac1 activity and cell invasion in the transfected cells were observed.     Results    The intensity of CrkⅠ and Dock180 expression was consistent with each other in EOC tissues. Both were observed to be significantly higher in EOC than those in the BOT and normal ovary tissues(P0.05). No significant difference was found between BOT and Normal group either for CrkⅠor Dock180 expression(P0.05). In consistent with this result

Dock180 preferred to combine with CrkⅠ rather than with CrkⅡ in all 3 ovarian cancer cell lines. Furthermore

Crk knockdown cells presented with sustainable CrkⅠ expression depletion

significantly decreased Rac1 activity and cell invasion.     Conclusion    Crk might be involved in malignant potential of human EOC mainly through CrkⅠ/Dock180/Rac1 pathway.