The quantitative polymerase chain reaction results showed that BANCR was frequently overexpressed in cancer tissues and this overexpression was found to significantly correlate with lymph node metastasis and tumour stage. The ectopic expression of BANCR contributed to the migration of human CRC Caco-2 cells, whereas knockdown of BANCR inhibited the migration of the HCT116 cells in vitro. Further investigation into the underlying mechanisms responsible for the migratory effects revealed that BANCR induced the epithelial-mesenchymal transition (EMT) through an MEK/extracellular signal-regulated kinase-dependent mechanism as treatment with the MEK inhibitor, U0126 decreased migration and reversed the EMT in the BANCR-overexpressed HCT116 cells.