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MicroRNAs have been integrated into tumorigenic programs as either oncogenes or tumor suppressor genes. The miR-630 was reported to be deregulated and involved in tumor progression of several human malignancies. However, its expression regulation shows diversity in different kinds of cancers and its potential roles remain greatly elusive. Herein, we demonstrate that miR-630 is significantly suppressed in human breast cancer specimens, as well as in various breast cancer cell lines. In aggressive MDA-MB-231-luc and BT549 breast cancer cells, ectopic expression of miR-630 strongly inhibits cell motility and invasive capacity in vitro. Moreover, lentivirus delivered miR-630 bestows MDA-MB-231-luc cells with the ability to suppress cell colony formation in vitro and pulmonary metastasis in vivo. Further studies identify metadherin (MTDH) as a direct target gene of miR-630. Functional studies shows that MTDH contributes to miR-630-endowed effects including cell migration and invasion as well as colony formation in vitro. Taken together, these findings highlight an important role for miR-630 in the regulation of metastatic potential of breast cancer and suggest a potential application of miR-630 in breast cancer treatment.

To search the microRNAs (miRNA) which suppress metastasis of breast cancer, we utilize three well known micoRNA target prediction programs, Targetscan, Pictar and miRanda, to select the microRNAs that target the genes related to tumor metastasis. We chose MDA-MB-231 with high metastasis ability as the model to evaluate the effect of miRNAs on cell motility through Transwell migration assay. After the first round of screening, miR-129 is found to significantly inhibit the migration of MDA-MB-231 both in Transwell migration assay and wound healing assay. Furthermore, miR-129 also shows great suppressive ability to cell mobility and migration in another two breast cancer cell lines BT549 and MDA-MB-435s. Most importantly, miR-129 is down-regulated both in breast cancer tissues compared with the paired adjacent normal breast tissues, and in breast cancer cell lines compared with normal breast epithelial cell MCF10A (P < 0.05). These results indicate that over-expression of miR-129 could inhibit breast cancer motility and migration, and the down-regulation of miR-129 may participate in the breast cancer migration and metastasis.