Many reports have demonstrated that loss of E-cadherin expression or function leads to a more invasive phenotype, and restoration of E-cadherin by conventional means can inhibit cells invasion in many types of tumors [10] and [11]. We have shown that our selective saRNA can efficiently activate expression of E-cadherin in
CX-4945 cancer cells, thus we next sought to determine whether saRNA could inhibit migration and invasion of bladder cancer cells in vitro. Matrigel invasion assays and wound closure assays were performed to examine whether migration and invasion of the 5637 cells transfected with dsEcad-215 were inhibited. As shown in Fig. 2A and B, dsEcad-215 transfected cells exhibited a significant decrease in both motility and invasion compared to dsControl and mock. Twenty-four hours after creating scratch, the gaps in dsControl and mock groups were almost closed. In contrast, the speed of wound closure was significantly slower in dsEcad-transfected cells, remaining open at 24 h after wound induction ( Fig. 2C). Viability of 5637
cells was assessed at 72 h by MTT assay to determine whether the decreased migration and invasion of cells with dsEcad-215 could be due to a change in cell proliferation. Results showed that viability of dsEcad-215 transfected cells was not significantly different from that of the cells with dsControl and mock (P > 0.05) (data not shown).
