Abstract: Objective :To observe the relationship between the expression of tumor suppressor gene TIP30 and of VEGF in human HCC tissues and its cell lines, and to analyze the mechanism of tumor metastasis inhibition effect of TIP30. Methods :Immunohistochemistry was used to detect the expression of TIP30 and VEGF protein. VEGF secretion in hepatocellular cell culture medium was detected using ELISA. Detection of VEGF transcription was conducted by RT-PCR. Results :(1) Of the 24 HCC specimens, the expression of TIP30 protein in 11 cases was reduced significantly compared to that in paraneoplastic tissues, and eight cases in the 11 specimen showed enhancement of the VEGF expression level. In the other 13 cases having no significant difference of TIP30 expression, the VEGF expression level was enhanced in four. There was a correlationship between the expression of TIP30 and of VEGF in HCC tissues (P<0.05). (2) Twelve hours after infection of adenovirus, there was no significant difference for expression level of VEGF in the hepatocellular cell culture medium, and 24 h after the infection, it began()decrease in the Ad-TIP30 group and there was a significant difference in the controls (P<0.01). It was also demonstrated, by RT-PCR detection, that the VEGF transcription was reduced 48h after Ad -TIP30 infection compared to the controls. Conclusions :There exist a positive correlation between the expression of TIP30 and of VEGF in the HCC tissues, and in the highmetastatic human HCC cell line ectogenic TIP30 gene introduction with high level could inhibit the expression or transcription of VEGF. So it can be speculated that the suppressor effect of TIP 30 gene for tumor metastasis may be partially completed through down-regulation of the VEGF expression, then consecutively inducing the vessel formation depression. So, it maybe provide a new target for anti-angiostatic therapy for malignant tumor invasion.