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Bmi-1 regulates epithelial-to-mesenchymal transition to promote migration and invasion of breast cancer cells
Authors:Haiyu Li  Fangzhou Song  Xingfeng Chen  Yun Li  Jianjun Fan  Xiangmei Wu
Affiliation:1.Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, 400016, China;2.Department of Biochemistry and Molecular Biology, Chongqing Medical University, Chongqing, 400016, China
Abstract:
Breast cancer is a highly invasive and metastatic disease. Recent studies report that breast cancer cells that have undergo epithelial-to-mesenchymal transition (EMT) obtain malignant characteristic, however, the molecular mechanism underlying this transition are poorly understood. Here, we found that over-expression associated with the process of breast cancer and that high B-cell-specific moloney murine leukemia virus insertion site 1 (Bmi-1) levels predict shorter survival of breast cancer patients. We demonstrate that Bmi-1 regulates EMT and the migration of breast cancer cells. RNA interference-mediated knockdown Bmi-1 expression restored E-cadherin expression and cell-cell junction formation in breast cancer cells, suppressing cell migration and invasion. In contrast, the over-expression of Bmi-1 decreased the expression of the epithelial mark (E-cadherin) but increased the mesenchymal makers (N-cadherin and vimentin) in breast cancer cells.
Keywords:Bmi-1   EMT   breast cancer   migration   invasion
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