MicroRNAs (miRNAs or miR) have been integrated into tumorigenic programs as 
either oncogenes or tumor suppressor genes. The miR-124 was reported to be 
attenuated in several tumors, such as glioma, medulloblastoma and hepatocellular 
carcinoma. However, its role in cancer remains greatly elusive. In this study, 
we show that the miR-124 expression is significantly suppressed in human breast 
cancer specimens, which is reversely correlated to histological grade of the 
cancer. More intriguingly, ectopic expression of miR-124 in aggressive breast 
cancer cell lines MDA-MB-231 and BT-549 strongly inhibits cell motility and 
invasive capacity, as well as the epithelial-mesenchymal transition process. 
Also, lentivirus-delivered miR-124 endows MDA-MB-231 cells with the ability to 
suppress cell colony formation in vitro and pulmonary metastasis in vivo. 
Further studies have identified the E-cadherin transcription repressor Slug as a 
direct target gene of miR-124; its downregulation by miR-124 increases the 
expression of E-cadherin, a hallmark of epithelial cells and a repressor of cell 
invasion and metastasis. Moreover, knockdown of Slug notably impairs the 
motility of MDA-MB-231 cells, whereas re-expression of Slug abrogates the 
reduction of motility and invasion ability induced by miR-124 in MDA-MB-231 
cells. These findings highlight an important role for miR-124 in the regulation 
of invasive and metastatic potential of breast cancer and suggest a potential 
application of miR-124 in cancer treatment.