Journal
MEDICAL ONCOLOGY
Volume 32, Issue 1, Pages -Publisher
HUMANA PRESS INC
DOI: 10.1007/s12032-014-0412-y
Keywords
B-Myb; EMT; Breast cancer; Migration; Invasion
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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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