B-Myb regulates snail expression to promote epithelial-to-mesenchymal transition and invasion of breast cancer cell.

Breast cancer is the leading cause of cancer death in women worldwide, which is closely related to metastasis. Recent studies argue that breast cancer cells that have undergone epithelial-to-mesenchymal transition (EMT) acquire aggressive malignant properties, but the molecular mechanisms underlying this transition are poorly understood. In this study, we found that siRNA-mediated attenuation of B-Myb expression restored E-cadherin expression and cell-cell junction formation in breast cancer cells, suppressing cell invasion, anchorage-independent growth, and tumor formation. In contrast, the forced B-Myb expression decreased the expression of the epithelial marker E-cadherin, but increased the mesenchymal markers in breast cancer cells. We found that B-Myb upregulated expression of the key EMT regulator snail and that it mediated EMT activation and cell invasion by B-Myb.