The relationship between sulfated lactosyl ceramide expressional level and hepatocellular carcinoma metastasis potential was investigated. By means of immunofluorescent staining and cell ELISA with monoclonal antibodies against sulfated lactosyl ceramide or galactocerebroside, it was observed that the expression of sulfated lactosyl ceramide in high metastasis hepatocarcinoma cells was significantly higher than those in low metastasis hepatocarcinoma cells. After the hepatocarcinoma cells with high metastatic potential were treated with 10 μmol/L retinoic acid, the level of sulfated lactosyl ceramide on the cell surface was significantly reduced (P＜0.05) to the level closing to the low metastatic hepatocarcinoma cells. The level of galactocerebroside which was the precursor of sulfated lactosyl ceramide did not change significantly. This indicated that the sulfation was inhibited after retinoic acid treatment. Therefore the cerebroside sulfotransferase gene were transferred into hepatocarcinoma cells and selected sulfated lactosyl ceramide-highly-expressed clones. Through adhesive assay, it was observed that the control cells were quite poor in adhesive to vitronectin and laminin, the transfected cells were significantly enhanced in the adhesion to vitronectin and laminin. After 45 minute incubation, the adhesive percentage of the cells was 3～4 time higher in CST-transfected cells than those in control cells. By animal experiments there were more metastatic foci in the liver or lymph nodes in CST-transfected groups than the control (P＜0.05). The results suggested that the high expression of SM3 in hepatocarcinoma cells promoted metastasis in nude mice and enhanced the adhesion to vitronectin.