Cadherins are transmembrane glycoproteins of cellular junctions that mediate calcium-dependent cell-cell adhesion and alterations in cadherin function have been implicated in tumorigenesis . Although the loss of E-cadherin has been seen as a hallmark of EMT, recent evidence have indicated that a gain of expression of N-cadherin but without E-cadherin change in tumour cells contributes directly to an increased invasive potential and is independently associated with an early stage of metastasis [44, 45]. The catenins, serving to link the cadherin to the cytoskeleton, can regulate alterations in cadherin function . Disruption of the connection between the cadherins and the cytoskeleton by mutations in β-catenin inactivates the adhesive function of E-cadherin in tumour cells and results in a non-adhesive phenotype. Thus, the increased expression of β-catenin is intimately related to the decline of E-cadherin . Our experiments confirm these findings. Similarly, in PLC-GRN/RBE-GRN cells, the up-modulation of N-cadherin, β-catenin and vimentin, as well as the downregulation of ZO-1while the decrease of E-cadherin were not detected in vitro. Therefore, we can also draw the conclusion that CsGRN induced the mesenchymal characteristics of PLC and RBE cells in responsible for cell invasion and metastasis. In contrast, in the liver of Balb/c mice immunised with rCsGRN protein, the upregulation of E-cadherin and downregulation of vimentin indicated the block of EMT progress. In other words, anti-CsGRN, a specific antibody produced by immunisation with rCsGRN protein, probably prevents the tumour cells from invasion and metastasis.