Abstract
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.
Highlights
Breast cancer remains to be the most common malignancy of women and causes 400,000 deaths annually worldwide [1]
We tested the expression of miR-630 by qRT-PCR in various breast cancer cell lines with a non-tumorigenic epithelial cell line MCF-10A as control
These results suggested that downregulation of miR-630 is a common event in breast cancer tissues, and it is inferred that miR-630 might involve in the pathogenesis of breast cancers
Summary
Breast cancer remains to be the most common malignancy of women and causes 400,000 deaths annually worldwide [1]. The majority of patients with metastatic disease will confront death between one and two years, even those treated with chemotherapy and caused tumor shrinkage at first [2]. Epithelial– mesenchymal transition (EMT) is thought to be necessary for the progression of original tumor cells to metastatic cells or at least an alternative program, the causes which endue tumor cells with the migration and invasion capability are not fully understood. The mechanism underlying this lethal step of cancer process remains to be clearly illustrated [2]
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