Abstract
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.
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Tao, D., Pan, Y., Jiang, G. et al. B-Myb regulates snail expression to promote epithelial-to-mesenchymal transition and invasion of breast cancer cell. Med Oncol 32, 412 (2015). https://doi.org/10.1007/s12032-014-0412-y
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DOI: https://doi.org/10.1007/s12032-014-0412-y