Organ-specific tumor cell adhesion to extracellular matrix (ECM) components and cell migration into host organs often involve integrin-mediated cellular processes.Direct integrin-mediated cell adhesion to ECM components in the space of Disse appears to be required for the successful liver metastatic formation of colon cancer.In the present study,human colon cancer HT-29 cells were transfected by liposome with integrin-β1 antisense oligodeoxynucleotide (ASODN).The integrin-β1 gene expression in HT-29 cells was significantly down-regulated.The migration of HT-29 cells was assayed using transwell cell culture chambers in vitro.The number of migrating HT-29 cells in experimental group was far less than that in control group (P＜0.05).The models of hepatic metastasis in nude mice were established by the intrasplenic injection of transfected HT-29 cells.Thirty days later,the nude mice were killed and the average number of hepatic metastases (4.00±0.93 per mouse),average volume (10.10±6.50 mm3 per mouse),average weight (0.0440±0.0008 g per mouse) in experimental group were remarkably reduced as compared with those in control group (P＜0.05).Integrin-β1 expression in the hepatic metastasis was studied by immunohistochemistry (SP).Positive cell percentage of hepatic metastases in experimental group was markedly decreased as compared with that in control group (P＜0.05).It was concluded that integrin-β1 may take part in hepatic metastasis,and down-regulation of integrin-β1 expression may play a key role in decreasing migration and hepatic metastasis of human colon carcinoma cells (HT-29).