Increasing evidence has revealed that thy-1 was a potential stem cell marker of liver cancer, but no data havebeen shown on how thy-1 regulates the pathophysiology of liver cancer, such as proliferation, apoptosis, invasionand migration. We previously demonstrated that thy-1 was expressed in about 1% of hepg2 cells, thy-1+ hepg2cells, but not thy-1-, demonstrating high tumorigenesis on inoculation 0.5x105 cells per BACA/LA mouse after2 months. In the present study, our results showed that higher expression of thy-1 occurs in 72% (36/50 cases)of neoplastic hepatic tissues as compared to 40% (20/50 cases) of control tissues, and the expression of thy-1 ishigher in poorly differentiated liver tumors than in the well-differentiated ones. In addition, thy-1 expressionwas detected in 85% of blood samples from liver cancer patients, but none in normal subjects or patients withcirrhosis or hepatitis. There was a significant negative correlation between thy-1expression and E-cadherinexpression (a marker of invasion and migraton), but not between thy-1 expression and AFP expression in all theliver cancer and blood samples. We further investigated the relationship between thy-1 and E- cadherin in livercancer hepg2 cell line which was transfected with pReceiver-M29/thy-1 eukaryotic expression vector followedby aspirin treatment. Lower expression of E- cadherin but higher expressions of thy-1 were detected in hepg2cells transfected with pReceiver-M29/thy-1. Taken together, our study suggested that thy-1 probably regulatesliver cancer invasion and migration.