To determine whether CsGRN could play any role in cancer cell migration, we carried out wound-healing assays. The results showed that PLC/RBE-GRN cells could induce significant cell migration when compared with PLC/RBE-GFP cells, respectively (Fig. 6). Similarly, transwell cell migration/invasion assay results indicated that the upregulation of CsGRN in PLC and RBE cells significantly increased migration/invasive activity compared with that in the control group (Fig. 7). Therefore, CsGRN could significantly improve the migration/invasion ability of CCA and HCC in vitro.Fig. 6 CsGRN promotes increased cell migration. Cell migration of PLC and RBE cells shown by wound-healing assay (a and c). Cells were observed using light microscope under 5× objective (scale-bar: 100 μm). Assays were performed in triplicate. Relative cell migration level was calculated by normalising to cell migration level at 0 h. ***P < 0.001, compared with the control group. Data are presented graphically in panels b and d Fig. 7Cell migration and invasion triggered by CsGRN in the transwell assay. PLC-GFP/GRN cells (a) or RBE-GFP/GRN cells (c) were suspended in serum-free media for 24 h. PLC-GFP cells and RBE-GFP cells were the negative control. Invasion assays were performed using Matrigel-coated membranes. The migration assay was similar to the invasion assay, except that the upper side of the membranes was not coated with the matrigel. Cells attached to the lower surface of the membranes at 24 h were counted under a light microscope. Cells were observed using a light microscope under a 10× objective (scale-bar: 100 μm). Ten random visual fields were selected to quantify the migration and invasion (b and d) using Image J software. **P < 0.01, ***P < 0.001, compared with control group